Analyzing 20 years of Resting-State fMRI Research: Trends and collaborative networks revealed.

Resting-state functional magnetic resonance imaging (rs-fMRI), initially proposed by Biswal et al. in 1995, has emerged as a pivotal facet of neuroimaging research. Its ability to examine brain activity during the resting state without the need for explicit tasks or stimuli has made it an integral component of brain imaging studies. In recent years, rs-fMRI has witnessed substantial growth and found widespread application in the investigation of functional connectivity within the brain. To delineate the developmental trajectory of rs-fMRI over the past two decades, we conducted a comprehensive analysis using bibliometric tool Citespace. Our analysis encompassed publication trends, authorship networks, institutional affiliations, international collaborations, as well as emergent themes in references and keywords. Our study reveals a remarkable increase in the volume of rs-fMRI publications over the past two decades, underscoring the burgeoning interest and potential within this field. Harvard University stands out as the institution with the highest number of research papers published in the realm of RS-fMRI, while the United States holds the highest overall influence in this domain. The recent emergence of keywords such as "machine learning" and "default mode," coupled with citation surges in reference to rs-fMRI, have paved new avenues for research within this field. Our study underscores the critical importance of integrating machine learning techniques into rs-fMRI investigations, offering valuable insights into brain function and disease diagnosis. These findings hold profound significance for the field of neuroscience and may furnish insights for future research employing rs-fMRI as a diagnostic tool for a wide array of neurological disorders, thus emphasizing its pivotal role and potential as a tool for investigating brain functionality.

Effects of smartphone-based hypnotic intervention for undergraduate students' shyness during the COVID-19 pandemic: A randomized controlled trial.

BACKGROUND: Since the outbreak of the COVID-19 pandemic, university students have been exposed to a heightened vulnerability towards developing psychological issues, such as psychological distress and shyness. Internet-based interventions offer a convenient avenue for scalability, thus prompting the development of a smartphone-based hypnotic intervention aimed at addressing shyness among university students. OBJECTIVE: We devised an innovative smartphone-based hypnotic intervention called mHypnosis to examine its impact on shyness among undergraduate students. Furthermore, we aimed to investigate whether the apprehension of negative evaluations before treatment could serve as a predictor for the effectiveness of the intervention on shyness. METHODS: Eighty students with high shyness scores were randomly assigned to the experimental group and the control group. Another 40 participants with low shyness score were selected as the baseline group. The Shyness Scale (SS), Fear of Negative evaluation scale (FNE), Self-Acceptance Questionnaire (SAQ), and Self-Esteem Scale (SES) were used to evaluate the effect of hypnotic intervention. RESULTS: Before the intervention, the scores of the experimental and control groups on the SS, FNE, SAQ, and SES were higher than those in the baseline group (p < 0.05). There was no significant difference in scores between the experimental and control group (p > 0.05). After the intervention, the scores of the SS, FNE, SAQ, and SES were significantly lower in the experimental group than those in the control group (p < 0.05). The pretest score of FNE could predict the shyness score after hypnotic intervention (B = 0.35, p < 0.05). CONCLUSION: Smartphone-based hypnotic intervention had a significant effect on ameliorating shyness during the COVID-19 pandemic; fear of negative evaluation can be a target for treating shyness.

Anomaly detection method for building energy consumption in multivariate time series based on graph attention mechanism.

A critical issue in intelligent building control is detecting energy consumption anomalies based on intelligent device status data. The building field is plagued by energy consumption anomalies caused by a number of factors, many of which are associated with one another in apparent temporal relationships. For the detection of abnormalities, most traditional detection methods rely solely on a single variable of energy consumption data and its time series changes. Therefore, they are unable to examine the correlation between the multiple characteristic factors that affect energy consumption anomalies and their relationship in time. The outcomes of anomaly detection are one-sided. To address the above problems, this paper proposes an anomaly detection method based on multivariate time series. Firstly, in order to extract the correlation between different feature variables affecting energy consumption, this paper introduces a graph convolutional network to build an anomaly detection framework. Secondly, as different feature variables have different influences on each other, the framework is enhanced by a graph attention mechanism so that time series features with higher influence on energy consumption are given more attention weights, resulting in better anomaly detection of building energy consumption. Finally, the effectiveness of this paper's method and existing methods for detecting energy consumption anomalies in smart buildings are compared using standard data sets. The experimental results show that the model has better detection accuracy.

AURKB Enhances Chromosomal Remodeling of Telomeric Genes and Accelerates Tumorigenesis of Uveal Melanoma.

Purpose: Uveal melanoma (UM) is the most common intraocular malignancy in adults developing liver metastases, threatening a patient's life. Current therapeutics failed to significantly improve the survival of patients with UM. Thus, the discovery of potent drugs is imminent. Methods: Integrated bioinformatic analysis of The Cancer Genome Atlas and immunohistochemistry staining of patients' tissues revealed the oncogenic role of aurora kinase B (AURKB) in UM. Drug sensitivity assays and an orthotopic intraocular animal model were used to test the efficacy of AURKB inhibitors. RNA sequencing and immunoblotting were performed to identify the downstream effector. A chromatin immunoprecipitation assay was conducted to elucidate AURKB's transcriptional regulation on the target gene. Results: AURKB was found overexpressed in patients with UM, resulting in a poor prognosis. Luckily, the AURKB-specific inhibitor, hesperadin, achieved prominent pharmacological efficiency in UM in vitro and in vivo. Mechanically, hesperadin compromised phosphorylation of histone H3 at serine 10 (H3S10ph) at the promoter of telomerase reverse transcriptase, accompanied by methylation of histone H3 at lysine 9. This methylated status of the promoter region forced chromatin condensation and consequently halted the transcription of telomerase reverse transcriptase. Conclusions: Collectively, our data demonstrated that AURKB inhibitors decelerated UM tumorigenesis by epigenetically silencing the expression of oncogenic telomerase reverse transcriptase, indicating AURKB as a potential therapeutic target in UM.

Body mass index increases the risk of breast cancer-related lymphedema at 6-18 months after surgery: a retrospective study.

PURPOSE: Breast cancer-related lymphedema (BCRL) is an incurable complication occurring after breast cancer treatment. The influence of obesity/overweight on the development of BCRL at different points after surgery was seldom verified. We aimed to determine the cut-off BMI/weight value associated with an increased risk of BCRL at different postoperative time in Chinese breast cancer survivors. METHODS: Patients who underwent breast surgery plus axillary lymph node dissection (ALND) were retrospectively evaluated. Disease and treatment characteristics of participants were collected. BCRL was diagnosed by circumference measurements. Univariate and multivariable logistic regression was used to assess the relationship of lymphedema risk with BMI/weight and other disease- and treatment-related factors. RESULTS: 518 patients were included. Lymphedema occurred more frequently among breast cancer patients with preoperative BMI ≥ 25 kg/m2 (37.88%) than among those with preoperative BMI < 25 kg/m2(23.32%), with significant differences at 6-12 and 12-18 months after surgery (χ2 = 23.183, P = 0.000; χ2 = 5.279, P = 0.022). By multivariable logistics analysis, preoperative BMI ≥ 30 kg/m2 presented a significantly greater risk of lymphedema than a preoperative BMI < 25 kg/m2 (OR [95% CI] = 2.928 [1.565, 5.480]). Other factors, including radiation (breast/chest wall + axilla vs. none: OR [95% CI] = 3.723[2.271-6.104]), was an independent risk factor for lymphedema. CONCLUSIONS: Preoperative obesity was an independent risk factor for BCRL in Chinese breast cancer survivors, and a preoperative BMI ≥ 25 kg/m2 indicated greater likelihood of lymphedema development within 6-18 months postoperatively.

Chromosomal instability-associated MAT1 lncRNA insulates MLL1-guided histone methylation and accelerates tumorigenesis.

Acquired chromosomal instability, especially copy number variations (CNVs), has been considered an important determinant of cancer progression and clinical survival. However, the functional role of aberrant CNV-induced lncRNAs in tumorigenesis remains unexplored. Here, we identify a CNV-induced MSC-antisense-transcript 1 (MAT1) lncRNA that plays an oncogenic role in promoting tumorigenesis of uveal melanoma in orthotopic and metastatic xenografts. In addition, our data suggest that MAT1 interrupts the interaction between the MLL1 complex and the PCDH20 promoter by forming an RNA-DNA triplex structure, subsequently abolishing H3K4 trimethylation and inactivating transcription of tumor suppressor PCDH20 to accelerate tumorigenesis. Our data show an intriguing insulation pattern of H3K4 histone modification in tumorigenesis mediated by a lncRNA, thereby providing an alternative mechanism for noncoding blockers in gene regulation.

Generation of αGal-enhanced bifunctional tumor vaccine.

Hepatocellular carcinoma (HCC) is a common malignant tumor with poor prognosis and high mortality. In this study, we demonstrated a novel vaccine targeting HCC and tumor neovascular endothelial cells by fusing recombinant MHCC97H cells expressing porcine α-1,3-galactose epitopes (αGal) and endorphin extracellular domains (END) with dendritic cells (DCs) from healthy volunteers. END+/Gal+-MHCC97H/DC fusion cells induced cytotoxic T lymphocytes (CTLs) and secretion of interferon-gamma (IFN-γ). CTLs targeted cells expressing αGal and END and tumor angiogenesis. The fused cell vaccine can effectively inhibit tumor growth and prolong the survival time of human hepatoma mice, indicating the high clinical potential of this new cell based vaccine.

Thymidine Kinase 1 Drives Skin Cutaneous Melanoma Malignant Progression and Metabolic Reprogramming.

Background: Thymidine kinase 1 (TK1) is a cell cycle-dependent kinase that catalyzes the addition of a gamma-phosphate group to thymidine. The protumorigenic role of TK1 has been reported in various malignancies. However, the role of TK1 in skin cutaneous melanoma (SKCM) remains unclear. This study aimed to explore the molecular function of TK1 in SKCM progression. Methods: Bioinformatics data were acquired from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO). Subcutaneous xenografts were established to observe the effect of TK1 knockdown on the proliferation of SKCM cells in vivo. RNA sequencing (RNA-seq; deposited in Sequence Read Archive, SRX10950283-SRX10950285 for A375 control cells and SRX10950286-SRX10950288 for TK1-silenced A375 cells) and immunoprecipitation-mass spectrometry (IP-MS) were used to analyze TK1-related genes and pathways. Seahorse XF Cell Mito tests and glycolysis stress assays were conducted for metabolic testing. Results: TK1 was upregulated in malignant SKCM compared to that in normal tissues and cell lines. Elevated expression of TK1 was associated with poor prognosis. In vitro and in vivo assays demonstrated that TK1 promoted the proliferation and migration of SKCM cells. Moreover, TK1 was strongly associated with multiple intracellular metabolic pathways, facilitating cell mitochondrial respiration and glycolysis in SKCM malignant progression. Conclusions: TK1 drives SKCM malignant progression and supports metabolic reprogramming, indicating that TK1 serves as a therapeutic target for SKCM.

A fluorescence aptasensor based on GSH@GQDs and RGO for the detection of Glypican-3.

Glypican-3 (GPC3), a heparin sulfate proteoglycan, is a potential diagnostic and therapeutic target for hepatocellular carcinoma. In this paper, a novel fluorescent aptasensor for GPC3 detection is constructed via glutathione@graphene quantum dots-labeled GPC3 aptamer (GSH@GQDs-GPC3Apt) as a fluorescence probe. First, GSH@GQDs is screened out with higher fluorescence intensity, which emits bright blue fluorescence under ultraviolet light. Then, the fluorescence-labeled GSH@GQDs-GPC3Apt probe is formed by the combination of amination GPC3Apt and GSH@GQDs using EDC/NHS coupled reaction. Under hydrogen bond and π-π interaction/stacking, the fluorescence of GSH@GQDs-GPC3Apt could be quenched by reductive graphene oxide (RGO) with the help of the photoinduced electron transfer and the fluorescence resonance energy transfer mechanism. In the presence of GPC3, the GSH@GQDs-GPC3Apt specifically recognizes and binds to GPC3, giving rise to the change of secondary structure of GPC3Apt to form the GPC3/GPC3Apt-GSH@GQDs complex, which would lead to the disintegration of the GSH@GQDs-GPC3Apt-RGO compound. Therefore, the energy transfer process is blocked and the fluorescence intensity is restored, enabling a highly sensitive response to GPC3. When the concentration of GPC3 is from 5.0 ng/mL to 150.0 ng/mL, the fluorescence recovery rate is well linearly related to GPC3 concentration with the limit of detection of 2.395 ng/mL (S/N = 3). This strategy shows recoveries from 98.31% to 101.89% in human serum samples and provides simple, fast and cheap analysis of GPC3, which suggests that it has great potential applications in clinical diagnosis for hepatocellular carcinoma.

Aptamer-based biosensors and application in tumor theranostics.

An aptamer is a short oligonucleotide chain that can specifically recognize targeting analytes. Due to its high specificity, low cost, and good biocompatibility, aptamers as the targeting elements of biosensors have been applied widely in non-invasive tumor imaging and treatment in situ to replace traditional methods. In this review, we will summarize recent advances in using aptamer-based biosensors in tumor diagnosis. After a brief introduction of the advantage of aptamers compared with enzyme sensors and immune sensors, the different sensing designs and mechanisms based on 3 signal transduction modes will be reviewed to cover different kinds of analytical methods, including: electrochemistry analysis, colorimetry analysis, and fluorescence analysis. Finally, the prospective advantages of aptamer-based biosensors in tumor theranostics and post-treatment monitoring are also evaluated in this review.

Comprehensive understanding of anchorage-independent survival and its implication in cancer metastasis.

Detachment is the initial and critical step for cancer metastasis. Only the cells that survive from detachment can develop metastases. Following the disruption of cell-extracellular matrix (ECM) interactions, cells are exposed to a totally different chemical and mechanical environment. During which, cells inevitably suffer from multiple stresses, including loss of growth stimuli from ECM, altered mechanical force, cytoskeletal reorganization, reduced nutrient uptake, and increased reactive oxygen species generation. Here we review the impact of these stresses on the anchorage-independent survival and the underlying molecular signaling pathways. Furthermore, its implications in cancer metastasis and treatment are also discussed.

Application of Molecular Nanoprobes in the Analysis of Differentially Expressed Genes and Prognostic Models of Primary Hepatocellular Carcinoma.

Analyzing hub genes related to tumorigenesis based on biological big data has recently become a hotspot in biomedicine. Nanoprobes, nanobodies and theranostic molecules targeting hub genes delivered by nanocarriers have been widely applied in tumor theranostics. Hepatocellular carcinoma (HCC) is one of the most common cancers, with a poor prognosis and high mortality. Identifying hub genes according to the gene expression levels and constructing prognostic signatures related to the onset and outcome of HCC will be of great significance. In this study, the expression profiles of HCC and normal tissue were obtained from the GEO database and analyzed by GEO2R to identify DEGs. GO terms and KEGG pathways were enriched in DAVID software. The STRING database was consulted to find protein-protein interactions between proteins encoded by the DEGs, which were visualized by Cytoscape. Then, overall survival associated with the hub genes was calculated by the Kaplan-Meier plotter online tool, and verification of the results was carried out on TCGA samples and their corresponding clinical information. A total of 603 DEGs were obtained, of which 479 were upregulated and 124 were downregulated. PPI networks including 603 DEGs and 18 clusters were constructed, of which 7 clusters with MCODE score ≥3 and nodes ≥5 were selected. The 5 genes with the highest degrees of connectivity were identified as hub genes, and a prognostic model was constructed. The expression and prognostic potential of this model was validated on TCGA clinical data. In conclusion, a five-gene signature (TOP2A, PCNA, AURKA, CDC20, CCNB2) overexpressed inHCC was identified, and a prognostic model was constructed. This gene signature may act as a prognostic model for HCC and provide potential targets of nanotechnology.

Dose-Dependent Carbon-Dot-Induced ROS Promote Uveal Melanoma Cell Tumorigenicity via Activation of mTOR Signaling and Glutamine Metabolism.

Uveal melanoma (UM) is the most common intraocular malignant tumor in adults and has a low survival rate following metastasis; it is derived from melanocytes susceptible to reactive oxygen species (ROS). Carbon dot (Cdot) nanoparticles are a promising tool in cancer detection and therapy due to their unique photophysical properties, low cytotoxicity, and efficient ROS productivity. However, the effects of Cdots on tumor metabolism and growth are not well characterized. Here, the effects of Cdots on UM cell metabolomics, growth, invasiveness, and tumorigenicity are investigated in vitro and in vivo zebrafish and nude mouse xenograft model. Cdots dose-dependently increase ROS levels in UM cells. At Cdots concentrations below 100 µg mL-1, Cdot-induced ROS promote UM cell growth, invasiveness, and tumorigenicity; at 200 µg mL-1, UM cells undergo apoptosis. The addition of antioxidants reverses the protumorigenic effects of Cdots. Cdots at 25-100 µg mL-1 activate Akt/mammalian target of rapamycin (mTOR) signaling and enhance glutamine metabolism, generating a cascade that promotes UM cell growth. These results demonstrate that moderate, subapoptotic doses of Cdots can promote UM cell tumorigenicity. This study lays the foundation for the rational application of ROS-producing nanoparticles in tumor imaging and therapy.

An Artificial CTCF Peptide Triggers Efficient Therapeutic Efficacy in Ocular Melanoma.

Although CCCTC binding factor (CTCF) has been demonstrated to play a variety of often contradictory roles in tumorigenesis, little is known about its function in the tumorigenesis of ocular melanoma. Here, we generated two artificial CTCF peptides (Decoy-CTCFs) combining the zinc finger domain of wild-type CTCF and artificial marker region. This Decoy-CTCF retained the DNA binding region but lost the functional regions of wild-type CTCF. Transferring artificial CTCF into ocular melanoma cells suppressed proliferation and migration in the tumor cells, while no effect was observed in normal cells. Intriguingly, we first showed that decoy-CTCF inhibited tumorigenesis by preventing the histone acetyltransferase EP300 from binding to the promoter of SELL. Thus SELL was a novel oncogene in the tumorigenesis of ocular melanoma. These studies provide efficient decoy CTCF-based therapeutic concept in malignant ocular melanoma and reveal the potential mechanism underlying decoy-based tumor therapy.

Dinutuximab Synergistically Enhances the Cytotoxicity of Natural Killer Cells to Retinoblastoma Through the Perforin-Granzyme B Pathway.

PURPOSE: Conventional chemotherapy and enucleation usually fail to cure advanced retinoblastoma. We investigated the retinoblastoma immune microenvironment and the efficacy of the combination of dinutuximab and CD16-expressing NK-92MI (NK-92MIhCD16-GFP) cells on retinoblastoma cells in this study. PATIENTS AND METHODS: Immunohistochemistry and flow cytometry (FC) were performed to assess the expression level of GD2 in retinoblastoma tissues and cells. Gene set enrichment analysis (GSEA), immunohistochemisrztry and immunocytochemistry were conducted to assess the retinoblastoma immune microenvironment and the integrity of the blood-retinal barrier (BRB). After overexpressing CD16 in NK-92MI cells, fluorescence-activated cell sorting (FACS) was applied to select the positive subpopulation. LDH assays and FC were used to detect LDH release and apoptosis in retinoblastoma cells subjected to a combination of dinutuximab and NK-92MIhCD16-GFP cells. Finally, the release of perforin-granzyme B and the expression of CD107a in NK-92MIhCD16-GFP stimulated by retinoblastoma cells were assessed via enzyme-linked immunosorbent assays (ELISAs) and FC in the presence of dinutuximab or an isotype control. RESULTS: GD2 was heterogeneously expressed in retinoblastoma tissues and cell lines and positively correlated with proliferation and staging. GSEA revealed the immunosuppressive status of retinoblastoma microenvironment. The immune cell profile of retinoblastoma tissues and vitreous bodies suggested BRB destruction. LDH release and apoptosis in retinoblastoma cells caused by NK-92MIhCD16-GFP cells were significantly enhanced by dinutuximab. Finally, the release of perforin-granzyme B and the expression of CD107a in NK-92MIhCD16-GFP cells stimulated by retinoblastoma cells were obviously increased by dinutuximab. CONCLUSION: This study indicates that retinoblastoma impairs the integrity of the BRB and contributes to dysregulated immune cell infiltrates. GD2 is a specific target for natural killer (NK) cell-based immunotherapy and that the combination of dinutuximab and NK-92MIhCD16-GFP cells exerts potent antitumor effects through antibody-dependent cell-mediated cytotoxicity.

Study of Cinobufagin as a Promising Anticancer Agent in Uveal Melanoma Through Intrinsic Apoptosis Pathway.

Uveal melanoma (UM) is the most common primary intraocular carcinoma in adults. Cinobufagin, secreted by the Asiatic toad Bufo gargarizans, is a traditional Chinese medicine, widely used in tumor treatment. Here, we explored the potential antitumor function of cinobufagin and investigated its biochemical mechanisms in UM cells. The antitumor potential of cinobufagin was determined via cell viability, cell cycle, and apoptosis assays. Colony formation assays confirmed that cinobufagin exerted potent antitumor activity in a dose-dependent manner. We found that cinobufagin could induce cell apoptosis and upregulate the expression of cleaved caspase-3, cleaved poly(ADP-ribose) polymerase (PARP), and cleaved caspase-9 in vivo and in vitro. In addition, after treatment with increased concentrations of cinobufagin, the intrinsic mitochondrial apoptosis pathway was also activated, which was demonstrated by increased cell apoptosis with increased expression of Bad and Bax, decreased expression of Bcl-2 and Bcl-xl, and reduced mitochondrial membrane potential (MMP) in OCM1 cells. Taken together, the results of this preclinical study suggest that cinobufagin can both inhibit cell survival and induce cell apoptosis in a dose-dependent manner in UM cells, which provides new insights into the biochemical mechanism of cinobufagin and its potential as a future chemotherapeutic agent for UM.

SKP2 targeted inhibition suppresses human uveal melanoma progression by blocking ubiquitylation of p27.

Background: SKP2 is considered an oncogene involved in various malignancies. SKP2 protein is a critical subunit of the SKP1-CUL1-F-box (SCF) E3 ligase complex which affects the cell cycle profoundly by specifically recognizing cell cycle regulators and mediating their ubiquitylation and proteasomal degradation. SKP2 dysfunction is characteristic of many tumor cells. However, its role in uveal melanoma (UM) has not been elucidated. Materials and methods: We analyzed the expressions of SKP2 in different UM cell lines compared with normal pigment cell by RNA-seq, RT-qPCR and Western blot. We then knocked down SKP2 in OM431 and MUM2B cells and confirmed its roles in cell proliferation via CCK8 assay. The sensitivity of cells to SKP2 inhibitor C1 (SKPin C1) in vitro was evaluated by CCK8 assay and colony formation assay, and the sensitivity of MUM2B cells to SKPin C1 in vivo was estimated using the nude mouse-based xenograft model. Western blot and Immunoprecipitation assay were performed to detect the change of p27 and its ubiquitylation level in UM cells treated with SKPin C1, respectively. Results: The results showed that SKP2 was significantly highly expressed in UM cells. SKP2 promoted the progression of UM and knockdown of SKP2 inhibited cell proliferation in UM cells. SKP2 inhibitor C1 that targets SKP2 essentially inhibits the growth of UM cells both in vivo and in vitro. SKP2 inhibitor C1 decreased the degradation of p27 by blocking ubiquitylation of p27, resulting in p27 accumulation and cell cycle arrest in UM cells. Conclusion: Our findings demonstrated that SKP2 targeted inhibition suppresses UM cell proliferation and provides new options and possibilities for targeted therapies in UM.

Altered expression profile of circular RNAs in conjunctival melanoma.

Aim: We aimed to explore the roles of circular RNA (circRNA) in conjunctival melanoma. Materials & methods: The altered circRNAs were identified by RNA sequencing. The function of one circRNA, circMTUS1, was explored by several experiments in conjunctival melanoma. Bioinformatic analyses and an RNA immunoprecipitation assay were performed to further study the downstream mechanism of circMTUS1. Results: We identified 9300 different circRNAs in conjunctival melanoma tissues compared with adjacent normal tissues. CircMTUS1 was upregulated in conjunctival melanoma. Silencing of circMTUS1 inhibited conjunctival melanoma proliferation in vitro and in vivo. CircMTUS1 may serve as an oncogene by binding to hsa-miR-622 and hsa-miR-1208 to regulate several tumor-related pathways. Conclusion: We demonstrated that circMTUS1 may serve as an oncogene to promote tumor proliferation.

Long Non-coding RNA LINC-PINT Suppresses Cell Proliferation and Migration of Melanoma via Recruiting EZH2.

Long non-coding RNAs (lncRNAs) have been identified as crucial regulators in many human cancers. Many lncRNAs show aberrant expression in cancer, and some of them play critical roles in tumor proliferation, invasion, and metastasis. However, the regulatory functions of lncRNAs in melanoma progression remain to be elucidated. We utilized the Real-time PCR methodology to determine the expression of LINC-PINT in melanoma cell lines. To evaluate the effect of LINC-PINT on tumorigenesis of melanoma, we used Cell Counting Kit-8 (CCK8) and colony formation assay. Flow cytometry assay was used to detect the function of LINC-PINT on cell cycle status. PINT-interacting proteins were identified by chromatin isolation using RNA purification (ChIRP). Microarray assay and bioinformatics analysis were used to find the potential target genes of LINC-PINT and the status of LINC-PINT target gene candidate was verified using chromatin immunoprecipitation assay (ChIP). LINC-PINT plays a role in suppressing the tumorigenicity of melanoma, which was further determined by xenograft model assay. LINC-PINT was significantly downregulated in melanoma tissues and cell lines. The overexpression of LINC-PINT in tumor cells resulted in significant tumor growth reduction and migration inhibition in A375, Mum2B and CRMM1 cells. Results based on the in vivo xenograft model were further consistent with the in vitro findings that LINC-PINT impeded growth and metastasis of melanoma cells. Microarray assay and bioinformatics analysis indicated that CDK1, CCNA2, AURKA, and PCNA were potential targets of LINC-PINT. In conclusion, LINC-PINT inhibits the tumorigenicity of melanoma through recruiting EZH2 to the promoter of its target genes, leading to H3K27 trimethylation and epigenetic silencing of target genes. LINC-PINT may serve as a novel diagnostic and therapeutic target for melanoma.

Factors promoting resilience among breast cancer patients: a qualitative study.

OBJECTIVE: The purpose of this study was to investigate resilience factors that helped Chinese breast cancer patients adapt to the trauma in the traditional Chinese cultural context. METHOD: Checklist-guided in-depth interviews were conducted on 15 Chinese breast cancer patients recruited from two affiliated teaching hospitals. All had adapted to the illness successfully. All interviews were guided by checklist-guided interview guidelines based on the social ecosystem theory. They were recorded digitally and transcribed verbatim. Data analysis was performed using published content analysis approach. FINDINGS: The main themes found to be relevant included hope for rehabilitation, hardiness, confidence in situation, optimistic attitude to the disease, gratitude to supporters, mastery of life. Each level of these individual resource interacted with each other, which was consistent with the micro system of social ecosystem theory. CONCLUSION: This study showed that individual resource played a significant role in helping the Chinese breast cancer patients deal with the illness. There is a clear need to develop a comprehensive evaluation system to help clinical nurses assess patients' individual resource and promote better adaption to breast cancer.