Enhancing the performance of AlGaN-based DUV-LEDs with multifocal laser stealth dicing.

In this study, AlGaN-based deep-ultraviolet light-emitting diodes (DUV-LEDs) processed via standard laser dicing (SLD) and multifocal laser stealth dicing (MFLSD) were investigated. Adopting the MFLSD technology would generate a roughing surface rather than the V-shaped grooves on the sidewall of 508 × 508 µm2 DUV-LEDs, which would reduce the forward operating voltage and increase the wall-plug efficiency, light output power, and far-field radiation patterns of these devices. In addition, the wavelength shift, far-field patterns, and light-tracing simulation results of the DUV-LEDs processed with SLD and MFLSD were clearly demonstrated and analyzed. Accordingly, it was observed that the MFLSD process provided more possibilities for photon escape to increase the light extraction efficiency (LEE) of DUV-LEDs, thus decreased the wavelength-redshift and junction temperature in DUV-LEDs. These results provide a reference for advanced nano-processing practices implemented during the fabrication of semiconductor devices.

Integrated bioinformatics analysis identified leucine rich repeat containing 15 and secreted phosphoprotein 1 as hub genes for calcific aortic valve disease and osteoarthritis.

Calcific aortic valve disease (CAVD) and osteoarthritis (OA) are common diseases in the ageing population and share similar pathogenesis, especially in inflammation. This study aims to discover potential diagnostic and therapeutic targets in patients with CAVD and OA. Three CAVD datasets and one OA dataset were obtained from the Gene Expression Omnibus database. We used bioinformatics methods to search for key genes and immune infiltration, and established a ceRNA network. Immunohistochemical staining was performed to verify the expression of candidate genes in human and mice aortic valve tissues. Two key genes obtained, leucine rich repeat containing 15 (LRRC15) and secreted phosphoprotein 1 (SPP1), were further screened using machine learning and verified in human and mice aortic valve tissues. Compared to normal tissues, the infiltration of immune cells in CAVD tissues was significantly higher, and the expressions of LRRC15 and SPP1 were positively correlated with immune cells infiltration. Moreover, the ceRNA network showed extensive regulatory interactions based on LRRC15 and SPP1. The authors' findings identified LRRC15 and SPP1 as hub genes in immunological mechanisms during CAVD and OA initiation and progression, as well as potential targets for drug development.

Application of Nanomedicine in Tumor Targeting Inflammatory Pathway.

Given the threat of ever-growing cancer morbidity, it is a cutting-edge frontier for multiple disciplines to apply nanotechnology in cancer therapy. Nanomedicine is now perpetually influencing the diagnosis and treatment of cancer. Meanwhile, tumorigenesis and cancer progression are intimately associated with inflammation. Inflammation can implicate in various tumor progression via the same or different pathways. Therefore, current nanomedicines exhibit tumor-suppressing function through inflammatory pathways. At present, the comprehensive understanding and research on the mechanism of various nanoparticles in cancer treatment are still in progress. In this review, we summarized the applications of nanomedicine in tumor-targeting inflammatory pathways, suggesting that nanoparticles could be a budding star for cancer therapy.

Clinical research progress of novel antituberculosis drugs on multidrug-resistant tuberculosis.

Multidrug-resistant tuberculosis (MDR-TB) has become a critical challenge to public health, and the prevention and treatment of MDR-TB are of great significance in reducing the global burden of tuberculosis. How to improve the effectiveness and safety of chemotherapy for MDR-TB is a pressing issue that needs to be addressed in tuberculosis control efforts. This article provides a comprehensive review of the clinical application of new antituberculosis drugs in MDR-TB, aiming to provide a scientific basis for the prevention and treatment strategy of MDR-TB.

Impacts of p-GaN layer thickness on the photoelectric and thermal performance of AlGaN-based deep-UV LEDs.

The effects of different p-GaN layer thickness on the photoelectric and thermal properties of AlGaN-based deep-ultraviolet light-emitting diodes (DUV-LEDs) were investigated. The results revealed that appropriate thinning of the p-GaN layer enhances the photoelectric performance and thermal stability of DUV-LEDs, reducing current crowding effects that affect the external quantum efficiency and chip heat dissipation. The ABC + f(n) model was used to analyse the EQE, which helped in identifying the different physical mechanisms for DUV-LEDs with different p-GaN layer thickness. Moreover, the finite difference time domain simulation results revealed that the light-extraction efficiency of the DUV-LEDs exhibits a trend similar to that of damped vibration as the thickness of the p-GaN layer increases. The AlGaN-based DUV-LED with a p-GaN layer thickness of 20 nm exhibited the best photoelectric characteristics and thermal stability.

Multimodality imaging in diagnosing lipomatous atrial septal hypertrophy with atrial septal defect: a case report.

Background: Lipomatous atrial septal hypertrophy (LASH) with atrial septal defect (ASD) is a rare congenital anomaly. Although LASH is a histologically benign cardiac lesion characterized by excessive fat deposition in the interatrial septum that spares the fossa ovale, it has been associated with supraventricular arrhythmias or sick sinus syndrome. Application of multimodal imaging is crucial for accurate diagnosis, appropriate treatment of LASH with ASD, and follow-up. Case summary: A 68-year-old female patient presented with recurrent chest tightness and palpitation. Multimodal imaging revealed the characterizations of LASH and ASD. Two-dimensional transesophageal echocardiography showed a "dumbbell"-shaped involvement of the cephalad and caudal regions with sparing of a single secundum ASD. The septum with a brightness feature is an uncommon condition characterized by the deposition of unencapsulated fat cells in the atrial septum. Real-time four-dimensional transesophageal echocardiography reflected the lipomatous hypertrophy of the atrial septum and an oval-shaped ASD. Cardiac computer tomography angiography later confirmed this finding. The patient achieved a good clinical response with an ASD percutaneous occlusion guided by intracardiac echocardiography (ICE). Conclusion: This case demonstrates a LASH combined with ASD. Multimodality imaging can provide an accurate diagnosis and may guide the procedure for precise occlusion.

Carbon Nanodots Attenuate Lipid Peroxidation in the LDL Receptor Knockout Mouse Brain.

Abnormal cholesterol metabolism can lead to oxidative stress in the brain. Low-density lipoprotein receptor (LDLr) knockout mice are models for studying altered cholesterol metabolism and oxidative stress onset in the brain. Carbon nanodots are a new class of carbon nanomaterials that possess antioxidant properties. The goal of our study was to evaluate the effectiveness of carbon nanodots in preventing brain lipid peroxidation. LDLr knockout mice and wild-type C57BL/6J mice were treated with saline or 2.5 mg/kg bw of carbon nanodots for a 16-week period. Brains were removed and dissected into the cortex, midbrain, and striatum. We measured lipid peroxidation in the mouse brain tissues using the Thiobarbituric Acid Reactive Substances Assay and iron and copper concentrations using Graphite Furnace Atomic Absorption Spectroscopy. We focused on iron and copper due to their association with oxidative stress. Iron concentrations were significantly elevated in the midbrain and striatum of the LDLr knockout mice compared to the C57BL/6J mice, whereas lipid peroxidation was greatest in the midbrain and cortex of the LDLr knockout mice. Treatment with carbon nanodots in the LDLr knockout mice attenuated both the rise in iron and lipid peroxidation, but they had no negative effect in the C57BL/6J mice, indicating the anti-oxidative stress properties of carbon nanodots. We also assessed locomotor and anxiety-like behaviors as functional indicators of lipid peroxidation and found that treatment with carbon nanodots prevented the anxiety-like behaviors displayed by the LDLr knockout mice. Overall, our results show that carbon nanodots are safe and may be an effective nanomaterial for combating the harmful effects caused by lipid peroxidation.

The regulatory role of LncRNA HCG18 in various cancers.

As a member of long non-coding RNAs (lncRNAs), LncRNA HLA complex group 18 (HCG18) has recently become the focus of cancer research. As outlined in this review, LncRNA HCG18 has been reported to be dysregulated in various cancers development and appears to be activated in a variety of tumors, including clear cell renal cell carcinoma (ccRCC), colorectal cancer (CRC), gastric cancer (GC), hepatocellular carcinoma (HCC), laryngeal and hypopharyngeal squamous cell carcinoma (LHSCC), lung adenocarcinoma (LUAD), nasopharyngeal cancer (NPC), osteosarcoma (OS), and prostate cancer (PCa). Furthermore, the expression of lncRNA HCG18 decreased in bladder cancer (BC) and papillary thyroid cancer (PTC). Overall, the presence of these differential expressions suggests the clinical value of HCG18 in cancer therapy. Additionally, lncRNA HCG18 influences various biological processes of cancer cells. This review summarizes the molecular mechanisms of HCG18 in cancer development, highlights reported the abnormal expression of HCG18 found in various cancer types, and aims to discuss the potential of HCG18 as a target for cancer therapy.

Identification of circRNA-miRNA-mRNA regulatory network and its role in cardiac hypertrophy.

BACKGROUND: Hypertrophic cardiomyopathy (HCM) is a grave hazard to human health. Circular RNA (circRNAs) and micro RNA (miRNAs), which are competitive endogenous RNA, have been shown to play a critical role inHCM pathogenicity. However, to a great extent, the biological activities of ceRNA in HCM pathophysiology and prognosis remain to be investigated. MATERIALS AND METHODS: By analyzing the expression files in the Gene Expression Comprehensive (GEO) database, differentially expressed (DE) circRNAs, miRNAs, and mRNAs in HCM were identified, and the target molecules of circRNAs and miRNAs were predicted. The intersection of the differentially expressed RNA molecules and the expected target was then calculated, and a ceRNA network was subsequently constructed using RNA molecules. Using Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses, the potential etiology was elucidated. qPCR was used to validate a portion of the hub gene using Angiotensin II to generate a cell hypertrophy model. RESULTS: Three large-scale HCM sample datasets were extracted from the GEO database. After crossing these molecules with their expected targets, the circRNA-miRNA-mRNA network had two DEcircRNAs, two DEmiRNAs, and thirty DEmRNAs, compared to normal tissues. Functional enrichment analysis of GO and KEGG demonstrated that many of the HCM pathways and mechanisms were associated with calcium channel release, which is also the primary focus of future research. The qPCR results revealed that circRNA, miRNA, and mRNA expression levels were different. They may include novel noninvasive indicators for the early screening and prognostic prediction of HCM. CONCLUSION: In this study, we hypothesized a circRNA-miRNA-mRNA regulation network that is closely related to the progression and clinical outcomes of HCM and may contain promising biomarkers and treatment targets for HCM.

LSINCT5: A Novel lncRNA in Cancers.

BACKGROUND: Long chain non-coding RNAs (lncRNA) are a kind of transcript that is around 200 nucleotides long and can engage in life activities via epigenetic, transcriptional, and post-transcriptional regulation. One of the key members of lncRNAs, long stress-induced noncoding transcripts 5 (LSINCT5), is localized at Chr 5p and has been reported to be abnormally expressed in a range of cancers. We present a comprehensive review of LSINCT5's aberrant expression and regulatory mechanisms in malignant tumors. METHODS: The included studies were retrieved and summarized through the PubMed database using the keywords "LSINCT5" and "Cancer" in detail. RESULTS: LSINCT5 behaves as an oncogene and abundantly expresses in malignant tumorigenesis and progression. By sponging microRNAs (miRNA), interacting with proteins, participating in cellular transduction, and being regulated by transcription factors, LSINCT5 can stimulate malignant behavior in a variety of tumor cells, including proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT). Furthermore, dysregulated LSINCT5 is usually associated with a poor prognosis. CONCLUSION: LSINCT5 has the potential to become a tumor diagnostic and prognostic marker, generating new access to clinical applications.

AGAP2-AS1: An Indispensable lncRNA in Tumors.

BACKGROUND: LncRNA has been found to participate in a variety of biological processes and play an important role in the occurrence and development of tumors. Therefore, it is of vital clinical value to study the relationship between lncRNA and tumor. It has been confirmed that lncRNA affects tumor progression through sponge mRNA, regulation of signal pathways and activity of oncogenes. Recent studies have shown that LncRNA AGAP2-AS1 is closely related to tumor, because this review focuses on the molecular mechanism of LncRNA AGAP2-AS1 affecting tumor progression. METHODS: The role of LncRNAAGAP2-AS1 in tumor was summarized by searching the literature related to LncRNAAGAP2-AS1 from PubMed in recent years. RESULTS: LncRNA AGAP2-AS1 is abnormally expressed as an oncogene in tumors, which participates in biological processes such as tumor proliferation, migration, invasion and autophagy. LncRNA AGAP2-AS1 plays an important role in tumorigenesis and development by binding to mRNA, regulating signal pathway and affecting protein activity, which suggests that AGAP2- AS1 may play a great potential value in the treatment of human cancer. CONCLUSION: The abnormal expression of LncRNAAGAP2-AS1 plays an important role in the progression of tumor and has a promising value in the treatment of tumor. Exploring the molecular mechanism of lncRNA AGAP2-AS1 is of indispensable significance for tumor treatment.

WDFY3-AS2: A Potential Prognostic Factor and Therapeutic Target Related to Cancer.

BACKGROUND: Abundant studies have shown that non-coding RNA is connected with tumor cell growth, migration and invasion. As a newly discovered non-coding RNA, WDFY3-AS2 has gradually emerged in the molecular mechanism of various tumors and has a potential prospect as a biological indicator of tumor prognosis. This review describes the pathophysiological mechanism and prognostic value of WDFY3-AS2 in different cancers. OBJECTIVE: This review reveals the changes and roles of WDFY3-AS2 in many tumors and cancers. The change of WDFY3-AS2 can be used as a cancer biomarker and plays an important role in improving tumor growth, migration and invasion. WDFY3-AS2 is unique because it can be considered a prognostic marker for many tumors and is of great significance for clinical diagnosis and treatment. WDFY3-AS2 shows the potential prognostic value and the prospect of therapeutic targets in various tumors. METHODS: PubMed reviewed the related literature to analyze and summarize the regulatory molecular mechanism of WDFY3-AS2 in various tumors and its value as a prognostic indicator. RESULTS: The abnormal expression of LncRNA WDFY3-AS2 in many cancers was connected with the poor prognosis of cancer patients, including diffuse glioma, hepatocellular carcinoma, ovarian cancer, esophageal cancer, triple-negative breast cancer, Clear Cell Renal Carcinoma, Esophageal squamous cell carcinoma, Lung adenocarcinoma, which participated in the recovery of orthodontic teeth. WDFY3-AS2 has revealed the cellular process of cancer cell growth, migration, and invasion. CONCLUSION: The molecular mechanism of LncRNA WDFY3-AS2 regulating tumor specifically proves that WDFY3-AS2 has a good prospect in the biological index of prognosis or clinical treatment target of cancer patients.

The Functions of EphA1 Receptor Tyrosine Kinase in Several Tumors.

BACKGROUND: Eph receptors tyrosine kinase (RTK) were identified in 1987 from hepatocellular carcinoma cell lines and were the largest known subfamily of RTK. Eph receptors can be divided into two categories, EphA and EphB, based on their structure and receptor-ligand specificity. EphA can be divided into 10 species (EphA 1-10) and EphB into 6 species (EphB1-6). Similarly, the ligands of Eph receptors are Ephrins. Ephrins also can be divided into Ephrin A and Ephrin B, of which there are five species(Ephrin-A1-5) and three species(Ephrin-B1-3). Among the Eph receptors, EphA1 has been the least studied so far. As far as we know, Eph receptors are involved in multiple pathologies, including cancer progression, tumor angiogenesis, intestinal environmental stability, the lymph node system, neurological disease, and inhibition of nerve regeneration after injury. There is a link between EphA1, integrin and ECM- related signal pathways. Ephrin-A1 is a ligand of the EphA1 receptor. EphA1 and ephrin-A1 functions are related to tumor angiogenesis. EphA1 and ephrin-A1 also play roles in gynecological diseases. Ephrin-A1 and EphA1 receptors regulate the follicular formation, ovulation, embryo transport, implantation and placental formation, which are of great significance for the occurrence of gynecological tumor diseases. EphA1 has been identified as an oncoprotein in various tumors and has been associated with the prognosis of various tumors in recent years. EphA1 is considered a driver gene in tumor genomics. There are significant differences in EphA1 expression levels in different types of normal tissues and tumors and even in different stages of tumor development, suggesting its functional diversity. Changes at the gene level in cell biology are often used as biological indicators of cancer, known as biomarkers, which can be used to provide diagnostic or prognostic information and are valuable for improving the detection, monitoring and treatment of tumors. However, few prognostic markers can selectively predict clinically significant tumors with poor prognosis. These malignancies are more likely to progress and lead to death, requiring more aggressive treatment. Currently available treatments for advanced cancer are often ineffective, and treatment options are mainly palliative. Therefore, early identification and treatment of those at risk of developing malignant tumors are crucial. Although pieces of evidence have shown the role of EphA1 in tumorigenesis and development, its specific mechanism is still unknown to a great extent. OBJECTIVE: This review reveals the changes and roles of EphA1 in many tumors and cancers. The change of EphA1 expression can be used as a biological marker of cancer, which is valuable for improving tumor detection, monitoring and treatment and can be applied to imaging. Studies have shown that structural modification of EphA1 could make it an effective new drug. EphA1 is unique in that it can be considered a prognostic marker in many tumors and is of important meaning for clinical diagnosis and operative treatment. At the same time, the study of the specific mechanism of EphA1 in tumors can provide a new way for targeted therapy. METHODS: Relevant studies were retrieved and collected through the PubMed system. After determining EphA1 as the research object, by analyzing research articles on EphA1 in the PubMed system in recent 10 years, we found that EphA1 was closely connected with the occurrence and development of tumors and further determined the references according to the influencing factors for review and analysis. RESULTS: EphA1 has been identified as a cancer protein in various tumors, such as hepatocellular carcinoma, nasopharyngeal carcinoma, ovarian cancer, gastric cancer, colorectal cancer, clear cell renal cell carcinoma, esophageal squamous cell carcinoma, breast cancer, prostate cancer and uveal melanoma. EphA1 is abnormally expressed in these tumor cells, which mainly plays a role in cancer progression, tumor angiogenesis, intestinal environmental stability, the lymph node system, nervous system diseases and gynecological diseases. In a narrow sense, EphA1 is especially effective in breast cancer in terms of gynecological diseases. However, the specific mechanism of EphA1 leading to the change of cancer cells in some tumors is not clear, which needs further research and exploration. CONCLUSION: RTK EphA1 can be used as a biomarker for tumor diagnosis (especially a prognostic marker), an indispensable therapeutic target for new anti-tumor therapies, and a novel anti-tumor drug.

Successful biventricular repair in a 14-year-old patient of asplenia with congenital heart disease syndrome.

Heterotaxy syndrome is a rare disease, and asplenia with congenital heart disease syndrome, also known as Ivemark syndrome, is a special form of heterotaxy syndrome. These patients usually have severe cardiovascular malformations and a poor prognosis. Their surgical outcomes are rarely satisfactory. We report the case of a 14-year-old patient who underwent successful corrective surgery treatment.

Atrial septal defect with a rare occupying lesion in heart.

BACKGROUND: Cardiac epicardium hemangiomas are exceedingly rare; however, they can cause significant hemodynamic impairment and large pericardial effusions. On rare occasion, cardiac tumors coexist with malformations of the heart. CASE PRESENTATION: We present the case of a 10-month-old female infant with a rare cardiac surface hemangioma coexisting with malformations of the heart. It revealed an atrial septal defect (ASD) coexisting with an abnormal occupying lesion with high echogenicity. It was 35*12*9 mm in size and was found in the anterior atrioventricular junction to the posterior atrioventricular junction at the bottom of the ventricular septum by transthoracic echocardiography. We performed surgical treatment of the atrial septal defect and performed biopsy with the occupying lesion. The histopathological examination reported a benign tumor as hemangioma. As far as we know, this is the first case in which cardiac surface hemangioma was found to coexist with an atrial septal defect. CONCLUSIONS: Cardiac epicardium hemangiomas is a rare solid tumor of the heart. If the mass is impossible to resect and does not cause hemodynamic impairment, only mass biopsy is possible.

Mechanobiology Platform Realized Using Photomechanical Mxene Nanocomposites: Bilayer Photoactuator Design and In Vitro Mechanical Forces Stimulation.

Mechanotransduction is the process by which cells convert external forces and physical constraints into biochemical signals that control several aspects of cellular behavior. A number of approaches have been proposed to investigate the mechanisms of mechanotransduction; however, it remains a great challenge to develop a platform for dynamic multivariate mechanical stimulation of single cells and small colonies of cells. In this study, we combined polydimethylsiloxane (PDMS) and PDMS/Mxene nanoplatelets (MNPs) to construct a soft bilayer nanocomposite for extracellular mechanical stimulation. Fast backlash actuation of the bilayer as a result of near-infrared irradiation caused mechanical force stimulation of cells in a controllable manner. The excellent controllability of the light intensity and frequency allowed backlash bending acceleration and frequency to be manipulated. As gastric gland carcinoma cell line MKN-45 was the research subject, mechanical force loading conditions could trigger apoptosis of the cells in a stimulation duration time-dependent manner. Cell apoptotic rates were positively related to the duration time. In the case of 6 min mechanical force loading, apoptotic cell percentage rose to 34.46% from 5.5% of the control. This approach helps apply extracellular mechanical forces, even with predesigned loading cycles, and provides a solution to study cell mechanotransduction in complex force conditions. It is also a promising therapeutic technique for combining physical therapy and biomechanics.

Decellularized bovine jugular vein and hand-sewn ePTFE valved conduit for right ventricular outflow tract reconstruction in children undergoing Ross procedure.

Background: The Ross procedure is recommended as an optimal aortic valve replacement (AVR) in children and young adults due to several advantages. Nevertheless, multiple reconstructions of the right ventricular outflow tract (RVOT) with new valve conduits have caused some concern regarding the durability of the Ross AVR. Decellularized bovine jugular vein conduit (BJVC) (DP-BJVC) and hand-sewn expanded polytetrafluoroethylene valved conduits (ePTFE VC) are widely employed to reconstruct the RVOT with satisfactory long-term outcomes. However, few studies have compared the safety and efficacy between the two valve conduits. We aimed to evaluate the early outcomes and report our single center experience in the application of these conduits. Methods: Twenty-two pediatric patients (aged < 18 years) who underwent Ross procedures with DP-BJVC and ePTFE VC in our center between 1 June, 2017 and 31 January, 2022 were enrolled. The Kaplan-Meier method was used to evaluate survival, freedom from RVOT reintervention, and freedom from RVOT graft dysfunction. Mixed-effects analysis with the Geisser-Greenhouse correction and Sidak's multiple comparisons test for post-hoc analysis was employed to compare the peak gradient across the conduit at varying follow-ups. Results: All patients were followed up in full. The total early survival rate was 90.9%; two patients in the DP-BJVC group died. There was no significant difference in early mortality, cross-clamp time (p = 0.212), in-hospital stay (p = 0.469), and RVOT graft thrombosis or endocarditis between the two groups. There was similarly no significant difference between Kaplan-Meier freedom from RVOT graft dysfunction curve (P = 0.131). The transprosthetic gradient gradually increased over time in both groups and was significantly higher in the DP-BJVC group at follow-up (P < 0.05). Conclusions: Both conduits show excellent early and midterm outcomes for RVOT reconstruction in the Ross procedure. We suggest that DP-BJVC is more suitable for infants, and ePTFE conduit is more suitable for older children who require larger conduits.

Individualized Analysis and Treatment of Difficult Weaning From Ventilation Following Open Cardiac Surgery in Young Children With Congenital Heart Disease.

Aims: The study explores the leading causes of postoperative extubation difficulties in pediatric patients (neonates and toddlers) with congenital heart diseases and establishes individualized treatment for different reasons. Method: We retrospectively analyzed medical records of 4,971 pediatric patients with congenital heart defects treated in three tertiary Congenital Heart Disease Centres in China from January 2005 to December 2020, from whom we selected those with difficulty extubation but successful weaning during the postoperative period. Next, we performed an analysis of risk factors and reported the combined experience of individualized treatment for successful extubation. Results: Seventy-five pediatric patients were identified in our database, among whom 23 had airway stenosis, 17 had diaphragmatic dysfunction, and 35 had pulmonary infection. The patients were all successfully weaned from the ventilator after an individualized treatment plan. In addition, the intubation time in the airway stenosis group was 17.7 ± 9.0, 33.6 ± 13.9 days in the diaphragmatic dysfunction group, and 11.9 ± 3.8 days in the pulmonary infection group. Conclusion: Given the primary reasons for difficult weaning following open-heart surgery in pediatric patients with congenital heart diseases, an individualized treatment scheme can achieve the ideal therapeutic effect where patients can be weaned faster with a shorter intubation period.

ITGA9: Potential Biomarkers and Therapeutic Targets in Different Tumors.

Integrins are a class of cell surface adhesion molecules composed of α subunit (ITGA) and ß subunit (ITGB). They belong to heterodimer transmembrane glycoproteins. Their main function in organisms is as the receptor of cell adhesion molecules (CAMs) and extracellular matrix (ECM). According to the current research integration analysis, integrin α9 (ITGA9) is one of the integrin subunits, and there are few studies on ITGA9 among integrins. ITGA9 can improve cell migration and regulate various cellular biological functions, such as tumor cell proliferation, adhesion, invasion, and angiogenesis. However, its abnormal expression mechanism in cancer and its specific role in tumor growth and metastasis are still unknown to a great extent. This review reveals the role of ITGA9 in the complex pathogenesis of many tumors and cancers, providing a new direction for the treatment of tumors and cancers. Relevant studies were retrieved and collected through the PubMed system. After determining ITGA9 as the research object, we found a close relationship between ITGA9 and tumorigenesis by analyzing the research articles on ITGA9 in the PubMed system in the last 15 years and further determined the references mainly based on the influencing factors of the articles. Thus, the role of ITGA9 in tumor and cancer genesis, proliferation, and metastasis was reviewed and analyzed. ITGA9 is an integrin subunit, which has been proved to be abnormally expressed in many tumors. After sorting and analyzing the research data, it was found that the abnormal expression of ITGA9 in a variety of tumors, including glioblastoma, rhabdomyosarcoma, melanoma, hepatocellular carcinoma, nasopharyngeal carcinoma, multiple myeloma, non-small cell lung cancer, and prostate cancer, was closely related to the proliferation, metastasis, adhesion, and angiogenesis of tumor cells. These results suggest that ITGA9 plays an important role in the occurrence and development of tumors. The integrin subunit ITGA9 may serve as a biomarker for the diagnosis of tumors and a potential therapeutic target for anti-tumor therapies.