CircSCUBE3 Reduces the Anti-gastric Cancer Activity of Anti-PD-L1.

The progression of gastric cancer (GC) is closely related to tumor immune escape. The research, therefore, studied the impact of possible circRNAs on the immune escape of GC tumors and the underlying mechanisms. Here, to explore circRNAs that may affect GC, the differential circRNAs in six normal gastric mucosal tissues and six GC samples (GSM2005868-GSM2005879) were analyzed through the bioinformatics website circmine, and hsa_circ_0076092 (circSCUBE3) was identified as the research object. In vitro assays revealed the functions of circSCUBE3 and its downstream miRNA/mRNA axis in GC cells. The effect of circSCUBE3 against PD-1 anti-tumor activity was evaluated in vivo. The relationship between circSCUBE3 and miR-744-5p, miR-744-5p, and SLC7A5 was identified by RNA immunoprecipitation and dual-luciferase reporter experiments. The effect of SLC7A5 on GC immune escape by regulating PD-L1 expression was assessed by co-culture system and flow cytometry. CircSCUBE3 was up-regulated in human GC tissues and GC cell lines. circSCUBE3 was associated with poor prognosis in GC patients. Functional experiments reported that circSCUBE3 knockdown could suppress GC immune escape. Mechanistically, circSCUBE3 bound to miR-744-5p, which further targeted SLC7A5, and SLC7A5 can affect GC immune escape by regulating PD-L1. Furthermore, in vivo assay manifested that circSCUBE3 attenuated the anti-tumor effect of PD-L1. Our study revealed the importance of the circSCUBE3/miR-744-5p/SLC7A5 axis in GC immune escape and anti-PD-1 resistance.

[MiR-744-5p inhibits the proliferation, invasion, and migration of clear-cell renal cell carcinoma cells by targeting CCND1].

OBJECTIVE: To explore the role of miR-744-5p/CCND1 axis in clear-cell renal cell carcinoma (ccRCC). METHODS: We examined the expression levels of miR-744-5p in 65 pairs of ccRCC and adjacent tissue specimens and in 5 ccRCC cell lines and human renal tubular epithelial (HK2) cells using qRT-PCR. The ccRCC cell lines 786-O and OSRC2 were transfected with miR-744-5p mimic, CCND1 mimic, or their negative control mimics, and the changes in cell proliferation, migration, and invasion were evaluated with CCK-8, wound healing, and Transwell assays. The downstream target molecules of miR-744-5p were predicted by bioinformatics analysis, and the expression level of CCND1 in ccRCC cells was verified by qRT-PCR and Western blotting. The relationship between miR-744-5p and CCND1 was further validated by dual luciferase reporter assay, and the role of the miR-744-5p/CCND1 axis in ccRCC was explored by rescue experiments. RESULTS: MiR-744-5p was significantly downregulated in ccRCC tissues and cell lines (all P < 0.05), and its overexpression inhibited the proliferation, migration, and invasion of ccRCC cells (all P < 0.05). Bioinformatics analysis and dual luciferase reporter assay showed that CCND1 was a downstream target of miR-744-5p. The results of rescue experiments showed that upregulation of CCND1 could partially reverse the inhibitory effect of miR-744-5p overexpression on ccRCC cell proliferation, migration, and invasion (all P < 0.05). CONCLUSION: MiR-744-5p inhibits the malignant phenotype of ccRCC cells by targeting CCND1, and the miR-744-5p/CCND1 axis may be a novel target for diagnosis and treatment of ccRCC.

MicroRNA-744-5p suppresses tumorigenesis and metastasis of osteosarcoma through the p38 mitogen-activated protein kinases pathway by targeting transforming growth factor-beta 1.

Osteosarcoma (OS) is the most common malignant bone tumor in children and adolescents. Accumulating evidence has revealed that microRNAs (miRNAs) play a crucial role in the progression of OS. In this study, we found that miR-744-5p was the least expressed miRNA in patients with OS by analyzing GSE65071 from the GENE EXPRESSION OMNIBUS (GEO) database. Through real-time quantitative PCR (qRT-PCR), western blotting, colony formation assay, 5-Ethynyl-2-Deoxyuridine (EdU) incorporation assay, transwell migration, and invasion assays, we demonstrated its ability to inhibit the proliferation, migration, and invasion of OS cells in vitro. According to the luciferase reporter assay, transforming growth factor-ß1 (TGFB1) was negatively regulated by miR-744-5p and reversed the effects of miR-744-5p on OS. Subcutaneous tumor-forming animal models and tail vein injection lung metastatic models were used in animal experiments, and it was found that miR-744-5p negatively regulated tumor growth and metastasis in vivo. Furthermore, rescue assays verified that miR-744-5p regulates TGFB1 expression in OS. Further experiments revealed that the p38 MAPK signaling pathway is involved in the miR-744-5p/TGFB1 axis. Generally, this study suggests that miR-744-5p is a negative regulator of TGFB1 and suppresses OS progression and metastasis via the p38 MAPK signaling pathway.

Long non-coding RNA NRSN2-AS1 facilitates tumorigenesis and progression of ovarian cancer via miR-744-5p/PRKX axis.

Newly discovered lncRNA neurensin-2 antisense RNA 1 (NRSN2-AS1) has not been well explored in cancers. Ovarian cancer (OV) is a primary gynecologic cancer worldwide and has the highest mortality rate among gynecologic cancers. Hence, the role and underlying mechanisms of NRSN2-AS1 in OV were worth investigating. According to the results of qantitative real-time polymerase chain reaction, NRSN2-AS1 displayed the remarkably high expression in OV cells, in contrast to human ovarian epithelial cells. Based on online database, the expression level of NRSN2-AS1 was significantly higher in OV tissues than that in normal ovarian tissues. The data from functional experiments indicated that NRSN2-AS1 knockdown inhibited OV cell malignant behaviors in vitro and OV tumor growth in vivo. Moreover, mechanism analysis unveiled that NRSN2-AS1 functioned as a miR-744-5p sponge to regulate PRKX expression in OV cells. The results of TOP/FOP flash and western blot assays suggested that NRSN2-AS1/miR-744-5p/PRKX axis modulated the activity of Wnt/ß-catenin signaling pathway. In summary, we validated NRSN2-AS1 functioned as a novel oncogenic lncRNA in OV and elucidated its specific molecular mechanism. This work might advance our understanding of OV and provide evidence for supporting NRSN2-AS1 as a potential biomarker for OV treatment.

MiR-744-5p inhibits the proliferation, invasion, and migration of clear-cell renal cell carcinoma cells by targeting CCND1 / 南方医科大学学报

OBJECTIVE@#To explore the role of miR-744-5p/CCND1 axis in clear-cell renal cell carcinoma (ccRCC).@*METHODS@#We examined the expression levels of miR-744-5p in 65 pairs of ccRCC and adjacent tissue specimens and in 5 ccRCC cell lines and human renal tubular epithelial (HK2) cells using qRT-PCR. The ccRCC cell lines 786-O and OSRC2 were transfected with miR-744-5p mimic, CCND1 mimic, or their negative control mimics, and the changes in cell proliferation, migration, and invasion were evaluated with CCK-8, wound healing, and Transwell assays. The downstream target molecules of miR-744-5p were predicted by bioinformatics analysis, and the expression level of CCND1 in ccRCC cells was verified by qRT-PCR and Western blotting. The relationship between miR-744-5p and CCND1 was further validated by dual luciferase reporter assay, and the role of the miR-744-5p/CCND1 axis in ccRCC was explored by rescue experiments.@*RESULTS@#MiR-744-5p was significantly downregulated in ccRCC tissues and cell lines (all P < 0.05), and its overexpression inhibited the proliferation, migration, and invasion of ccRCC cells (all P < 0.05). Bioinformatics analysis and dual luciferase reporter assay showed that CCND1 was a downstream target of miR-744-5p. The results of rescue experiments showed that upregulation of CCND1 could partially reverse the inhibitory effect of miR-744-5p overexpression on ccRCC cell proliferation, migration, and invasion (all P < 0.05).@*CONCLUSION@#MiR-744-5p inhibits the malignant phenotype of ccRCC cells by targeting CCND1, and the miR-744-5p/CCND1 axis may be a novel target for diagnosis and treatment of ccRCC.

LncRNA MNX1-AS1 promotes ovarian cancer process via targeting the miR-744-5p/SOX12 axis.

PURPOSE: Ovarian cancer (OC) is the most common malignancy in women with high mortality. Increasing studies have revealed that long non-coding RNA (lncRNA) MNX1-AS1 has a promoting effect on various cancers. However, the mechanisms of MNX1-AS1 in OC are still unclear. Therefore, this study focused on exploring the mechanisms of MNX1-AS1 in OC. MATERIALS AND METHODS: The expression of SOX12 at the protein level was detected by western blot. Cell proliferation was detected by CCK8 assay and colony formation assay. Cell cycle and cell apoptosis were detected by flow cytometry. Wound-healing assay, transwell assay and western blot were used to detect the ability of cell migration and invasion. The target binding was confirmed through the luciferase reporter assay. RESULTS: The expression of MNX1-AS1 was increased in OC tumor tissues and cells. Elevated MNX1-AS1 expression is associated with advanced stage and lower overall survival rate. Knockdown of MNX1-AS1 inhibited cell proliferation, migration and invasion, blocked cell cycle, and promoted cell apoptosis in SKOV-3 and OVCAR-3 cells. MNX1-AS1 was competitively binding with miR-744-5p, and its downstream target gene was SOX12. miR-544-5p expression was decreased, while SOX12 expression was increased in OC tumor tissues and cells. Overexpression of miR-744-5p inhibited cell proliferation, migration, invasion and promoted cell apoptosis in SKOV-3 and OVCAR-3 cells. CONCLUSION: MNX1-AS1 promoted the development of OC through miR-744-5p/SOX12 axis. This study revealed a novel mechanism of MNX1-AS1 in OC, which may provide a new treatment or scanning target for OC.

LINC00665 knockdown protects against cerebral ischemia-reperfusion injury.

LINC00665 has been reported to participate in several human diseases. However, the role of LINC00665 in cerebral ischemia-reperfusion (CI/R) is still unknown. This study is designed to investigate the role of LINC00665 in rats with CI/R injury. We established middle cerebral artery occlusion/ reperfusion (MCAO/R) rats model in vivo. PC12 cells treated with oxygen-glucose deprivation/reperfusion (OGD/R) were used to establish in vitro I/R model. RT-qPCR assay was adopted to assess the mRNA expression of LINC00665 and miR-744-5p. MTT assay was used to determine cell viability. The protein expression of Bax and Bcl-2 were detected by Western blot assay. The relationship between LINC00665 and miR-744-5p was confirmed by dual luciferase reporter assay and RNA immunoprecipitation (RIP). In this study, we found that LINC00665 was sharply up regulated in MCAO/R rats and PC12 cells treated with I/R. Functionally, LINC00665 knockdown attenuated oxidative damage in PC12 cells treated with I/R. Moreover, LINC00665 knockdown promoted cell viability, while inhibited cell apoptosis in PC12 cells treated with I/R. In addition, miR-744-5p was confirmed to be a target of LINC00665. LINC00665 knockdown was validated to project CI/R injury by sponging miR-744-5p expression.

LINC01116 boosts the progression of pituitary adenoma via regulating miR-744-5p/HOXB8 pathway.

Pituitary adenoma (PA) is one of the common intracranial tumors. In order to optimize status quo, seeking out potential biomarkers for pituitary adenoma diagnosis and treatment is urgent and important. Long non-coding RNAs (lncRNAs) have been related with progression of various cancers. Based on this reason and unknown role of long intergenic non-protein coding RNA 1116 (LINC01116) in pituitary adenoma, we aimed to explore the function and molecular mechanism of LINC01116 in pituitary adenoma. The RT-qPCR analysis showed that LINC01116 was abnormally overexpressed in pituitary adenoma cells. Down-regulated LINC01116 effectively suppressed cell proliferation and migration as well as epithelial-mesenchymal transition (EMT) progression in pituitary adenoma. Additionally, LINC01116 could competitively sponge miR-744-5p as shown by RIP, RNA pull down and luciferase reporter assays. Similarly, we also proved that homeobox B8 (HOXB8) was the target gene of miR-744-5p in pituitary adenoma cells. In the end, the rescue assays unmasked that HOXB8 could effectually reverse inhibition effect of LINC016 knockdown on pituitary adenoma cells proliferation, migration and EMT, further suggesting that LINC01116 expedited the pituitary adenoma progression by up-regulating HOXB8. Taken together, LINC01116 boosted the progression of pituitary adenoma cells via regulating miR-744-5p/HOXB8 pathway.

Long non-coding RNA LINC01116 is activated by EGR1 and facilitates lung adenocarcinoma oncogenicity via targeting miR-744-5p/CDCA4 axis.

BACKGROUND: Lung adenocarcinoma (LAD) is one of the most frequently diagnosed pathological categories of human lung cancer. Nevertheless, the link between long non-coding RNA (lncRNA) LINC01116 and LAD remains poorly investigated. METHODS: QRT-PCR and western blot were applied for quantifying the expression of RNAs and proteins. Both functional experiments assays in vitro and xenografts model in vivo were implemented for analyzing LINC01116 function in LAD while molecular relationship among RNAs was investigated via mechanism experiments. RESULTS: LINC01116 was expressed at an abnormally high level in LAD, which was induced by transcription activator EGR1. LINC01116 depletion restrained proliferation, migration and invasion, yet facilitated apoptosis of LAD cells. MiR-744-5p could bind to LINC01116. MiR-744-5p inhibitor reversed the inhibitory effects of silencing LINC01116 on LAD malignant behaviors. In addition, cell division cycle-associated protein 4 (CDCA4) shared binding sites with miR-744-5p. Silencing LINC01116 elicited decline in CDCA4 mRNA and protein levels. Moreover, CDCA4 up-regulation could counteract the biological effects of LINC01116 knockdown on LAD cells. CONCLUSION: Our data revealed that LINC01116 promoted malignant behaviors of LAD cells by targeting miR-744-5p/CDCA4 axis, implying the theoretical potential of LINC01116 as a novel target for LAD treatment.

Knocking down LINC01116 can inhibit the regulation of TGF-ß through miR-774-5p axis and inhibit the occurrence and development of glioma.

BACKGROUND: Many studies have shown that non-coding RNAs (ncRNAs), including long non-coding RNA (LncRNA) and micro RNA (miRNA), play a crucial regulatory role in glioma. LINC01116 is a newly discovered LncRNA, and the relationship between LncRNA and glioma is still under exploration. METHOD: LncRNAs with potential differences were screened through GEO database, and the expressions of LINC01116 and miR-744-5p/TGF-ß1 in glioma tissues were tested using qRT-PCR. Changes in proliferation and migration/invasion of glioma were tested using CCK-8 and transwell assay. The expression changes of TGF-ß1 were tested using qRT-PCR and Western blot. Targeted binding among LINC01116, miR-744-5p and TGF-ß1 was verified using double luciferase reporter, RNA Immunoprecipitation (PIR) and RNA pull-down experiments. The effect of LINC01116 on tumor growth was determined by tumor allografting test. RESULTS: GEO database and clinical research revealed that the expression level of LINC01116 in glioma increased, and the elevation of LINC01116 was closely related to the adverse prognosis of clinical patients. Functional experiments showed that the inhibition of LINC01116 could up-regulate miR-744-5p-mediated proliferation and metastasis of glioma cells. Western blot analysis and qRT-PCR analysis showed that LINC01116 regulated TGF-ß1 by mediating miR-744-5p. Further cell behavior experiments showed that LINC01116 acted as miR-744-5p sponge to inhibit proliferation and metastasis caused by TGF-ß1. Finally, the analysis of animal models in vivo showed that LINC01116 could regulate the tumor growth of glioma. CONCLUSION: LncRNA LINC01116 acts as an oncogene and promotes TGF-ß1 mediated proliferation and metastasis by acting as competitive endogenous RNA (ceRNA) in glioma.

LncRNA MNX1-AS1 Contributes to Laryngeal Squamous Cell Carcinoma Growth and Migration by Regulating mir-744-5p/bcl9/ß-Catenin Axis.

Increasing evidence has indicated that long noncoding RNAs (lncRNAs) are involved in the progression of laryngeal squamous cell carcinoma (LSCC). Here, we aimed to disclose the role of MNX1-AS1 in LSCC progression, and explore whether MNX1-AS1 participates in LSCC progression via targeting miR-744-5p to active BCL9/ß-catenin signaling. Sixty-five human LSCC tissues and the paracancerous normal tissues were recruited to determine the levels of MNX1-AS1, miR-744-5p and BCL9 using qRT-PCR. The interaction of miR-744-5p and MNX1-AS1/BCL9 was determined by using the RNA immunoprecipitation (RIP) assay and/or luciferase gene reporter assay. Cell viability, in vivo tumor formation, invasion and migration abilities were detected by MTT, Xenograft models and Transwell assays. MNX1-AS1 level was increased significantly in human LSCC tissues as compared with the normal tissues, which showed a positive correlation with BCL9 level while a negative correlation with miR-744-5p level. High level of MNX1-AS1 predicted a poor prognosis and an advanced clinical process in LSCC patients. miR-744-5p targeted upregulation weakened the luciferase activity of MNX1-AS1 and /BCL9, and downregulated their expression levels-wt, while showed no effect when the binding sites were mutated. Knockdown of MNX1-AS1 markedly weakened cell viability, migration, and invasion abilities, while BCL9 overexpression abolished these tendencies. In addition, MNX1-AS1 downregulation induced decreases in tumor volumes and weights in vivo, accompanied by reductions in BCL9, Ki-67 and ß-catenin expression and an increase in miR-744-5p expression. Collectively, this study reveals that MNX1-AS1 contributes to cell growth and migration by regulating miR-744-5p/BCL9/ß-catenin axis in LSCC.

miR-744-5p Inhibits Multiple Myeloma Proliferation, Epithelial Mesenchymal Transformation and Glycolysis by Targeting SOX12/Wnt/ß-Catenin Signaling.

PURPOSE: This study investigated the function and molecular mechanisms of miR-744-5p in multiple myeloma (MM). METHODS: miR-744-5p and SRY-related high-mobility-group box 12 (SOX12) expression in clinical tissues and MM cells was monitored by quantitative real-time polymerase chain reactions and Western blot. miR-744-5p expression in MM cells was regulated by transfection. Cell proliferation was researched by cell counting kit-8 assay and plate clone formation experiment. Transwell experiment was utilized for migration and invasion detection. Glycolysis test was conducted for the detection of glucose uptake and lactate production of MM cells. The relationship between miR-744-5p and SOX12 was determined by dual-luciferase reporter gene assay and RNA pull-down experiment. In vivo experiment was conducted using nude mice. RESULTS: miR-744-5p expression was reduced in MM patients (P<0.01). Low miR-744-5p expression was associated with lower 60-month survival in MM patients (P=0.0402). miR-744-5p overexpression inhibited MM cells proliferation, invasion, migration, glucose uptake, lactate production, and epithelial mesenchymal transformation (EMT) (P<0.01). miR-744-5p directly inhibited SOX12 expression. miR-744-5p silencing promoted MM cells proliferation, invasion, migration, glucose uptake, lactate production, and EMT by elevating SOX12 (P<0.01). miR-744-5p inhibited the growth of MM xenograft tumors in vivo (P<0.001). CONCLUSION: miR-744-5p inhibits MM cells proliferation, invasion, migration, EMT, and glycolysis by targeting SOX12/Wnt/ß-catenin.

Long non-coding RNA LINC01116 acts as an oncogene in prostate cancer cells through regulation of miR-744-5p/UBE2L3 axis.

BACKGROUND: Long non-coding RNA (lncRNA) has been confirmed to exert a critical effect on the progression of tumors, including prostate cancer. Previous literature has demonstrated LINC01116 involves in activities of multiple cancers. However, the underlying role of LINC01116 in prostate cancer remains unclear. METHODS: qRT-PCR measured the expression of LINC01116 in prostate cancer cells. EdU experiment was used to detect cell proliferation. Transwell assays detected cell migration and invasion. Immunofluorescence staining and western blot assays were utilized to measure EMT progress. The binding relationship between RNAs was confirmed by a series of mechanism assays. In addition, rescue experiments were conducted to verify the relationship among RNAs. RESULTS: LINC01116 was found to be highly expressed in prostate cancer cells. Functional assays indicated that inhibition of LINC01116 could suppress cell proliferation, migration, invasion and EMT progress. Also, miR-744-5p was proven to bind with LINC01116. Moreover, UBE2L3 was verified as the target gene of miR-744-5p. In rescue assays, we discovered that inhibited miR-744-5p or overexpressed UBE2L3 could offset the suppressive influence of silencing LINC01116 on prostate cancer cells. CONCLUSION: Our study suggested that lncRNA LINC01116 acted as an oncogene in prostate cancer and accelerated prostate cancer cell growth through regulating miR-744-5p/UBE2L3 axis.

Long noncoding RNA MNX1-AS1 functions as a competing endogenous RNA to regulate epithelial-mesenchymal transition by sponging MiR-744-5p in colorectal cancer.

Colorectal cancer (CRC) is the fourth most deadly cancer globally. Long noncoding RNA MNX1-AS1 has been proven to play a regulatory role in various human cancers. The present research aimed to explore the MNX1-AS1 function in CRC and the corresponding mechanism. A series of experiments were conducted to detect the effects of MNX1-AS1 and miR-744-5p on the biological function of CRC cells, including quantitative reverse transcription-polymerase chain reaction, CCK-8, transwell, wound healing assay, Western blot, and dual-luciferase report assay. MNX1-AS1 was elevated in CRC tissues and cell lines. Si-MNX1-AS1 inhibited cell viability, invasion, migration, and the protein expressions of N-cadherin and Vimentin but promoted the protein expression of E-cadherin. MiR-744-5p bound to MNX1-AS1. MiR-744-5p inhibitor had the opposite effect of si-MNX1-AS1. Cotransfection of miR-744-5p inhibitor and si-MNX1-AS1 recovered the effects mentioned above. In conclusion, MNX1-AS1/miR-744-5p axis plays a pivotal role in the viability, invasion, migration, and epithelial-mesenchymal transition of colorectal cancer cells.

miR-744-5p inhibits cellular proliferation and invasion via targeting ARF1 in epithelial ovarian cancer.

miR-744-5p has been demonstrated to play an important role in cancer progression. However, the functions of miR-744-5p in epithelial ovarian cancer (EOC) are not well clarified. In this study, our aim was to investigate the role of miR-744-5p and its underlying molecular mechanism in cell progression of EOC. EOC clinical tissues and matched adjacent ovarian epithelial tissues were collected from 18 patients. Tissues and cell lines were analyzed by qPCR or Western blot to investigate the expression of miR-744-5p and ARF1 in EOC. Cell proliferative capacity was assessed by CCK8 and colony formation assays. Wound healing and transwell assays were performed to evaluate cell migration and invasion. The potential binding relation between miR-744-5p and IRF1 was demonstrated by dual luciferase report assay. The results showed that expression of miR-744-5p was low in EOC clinical tissues and cells. Overexpression of miR-744-5p inhibited proliferation, migration, and invasion of EOC cells. Further mechanistic study identified that ARF1 is a target of miR-744-5p, which is negatively correlated with the expression of miR-744-5p, and overexpression of ARF1 could reverse the inhibition of miR-744-5p on the proliferation, migration, and invasion of EOC cells. Taken together, our results indicated that miR-744-5p attenuated EOC progression via targeting IRF1, providing potential guidance for the clinical treatment of ovarian cancer.

Long non-coding RNA LINC01116 regulated miR-744-5p/SCN1B axis to exacerbate lung squamous cell carcinoma.

BACKGROUND: Lung squamous cell carcinoma (LUSC) is a kind of lung cancer which possesses high morbidity and mortality. Long non-coding RNAs (lncRNAs) have been abundantly reported to participate in regulating cellular activities of various diseases, including cancers. LINC01116 was reported as a tumor promoter in some cancers, whereas its function has not been clarified in LUSC. OBJECTIVE: This exploration aimed to study the modulatory role of LINC01116 in LUSC. METHODS: The expressions of LINC01116, miR-744-5p and SCN1B were determined by RT-qPCR. CCK-8, EdU and transwell assays were conducted to evaluate the proliferative, migratory and invasive abilities of A549 and H1299 cells. The protein expression of SCN1B or EMT-associated proteins was examined through western blot assay. The interaction between miR-744-5p and LINC01116 (or SCN1B) was confirmed by RNA pull down and luciferase reporter assays. RESULTS: LINC01116 was up-regulated in LUSC tissues and cells, and LINC01116 repression limited the proliferative, migratory, invasive capabilities and EMT process in LUSC cells. In mechanism, LINC01116 directly interacted with miR-744-5p, and its expression was negatively correlated with miR-744-5p expression. SCN1B, overexpressed in LUSC tissues and cells, was proved to be targeted by miR-744-5p. Furthermore, SCN1B expression was in a negative association with miR-744-5p expression. At last, SCN1B amplification recovered the inhibitive effect of LINC01116 knockdown on cell proliferation, migration, invasion and EMT process in LUSC. CONCLUSION: LINC01116 regulated miR-744-5p/SCN1B axis to exacerbate LUSC, providing a helpful theoretic basis for the exploration of LUSC treatment.

miR-744-5p mediates lncRNA HOTTIP to regulate the proliferation and apoptosis of papillary thyroid carcinoma cells.

Papillary thyroid carcinoma (PTC) is the most common malignancy in thyroid. miR-744-5p plays an efficient role in various cancers, but its role in PTC remains unknown. In this work, we aimed to explore the function of miR-744-5p and the mechanism by which miR-744-5p acted in PTC. We observed that miR-744-5p expression was significantly declined in PTC tissues and cell lines. The high level of miR-744-5p is significantly associated with a better clinical picture of PTC patients. Overexpression of miR-744-5p inhibited the proliferation, arrested the cell cycle, and promoted the apoptosis in PTC cells. Oppositely, down-regulation of miR-744-5p reversed the above tendencies. We also found that miR-744-5p down-regulated its downstream genes c-myc and attenuated cell proliferation induced by c-myc. Long non-coding RNA (lncRNA) HOTTIP was found to be up-regulated and to act as an oncogene in PTC. In this study, miR-744-5p bound to HOTTIP and was negatively regulated by HOTTIP. In conclusion, miR-744-5p acts as a tumor suppressor to inhibit proliferation and promotes the apoptosis of PTC cells via targeting c-myc. Moreover, miR-744-5p expression interferes with lncRNA HOTTIP ability to promote proliferation and downregulate apoptosis in papillary thyroid carcinoma.

miR-744-5p Inhibits Non-Small Cell Lung Cancer Proliferation and Invasion by Directly Targeting PAX2.

Non-small cell lung cancer is one of the leading causes of cancer-related death worldwide. MicroRNAs have been characterized as critical regulators for cancer progression including non-small cell lung cancer. This work explored microRNA-744-5p expression in non-small cell lung cancer cell lines and normal cell line using quantitative real-time polymerase chain reaction. Connection of microRNA-744-5p and paired box 2 was analyzed with bioinformatic analysis, luciferase activity reporter assay, and Western blot. Effects of microRNA-744-5p or paired box 2 expression on non-small cell lung cancer cell behaviors were analyzed using a series of in vitro experiments. MicroRNA-744-5p was found to have decreased expression in non-small cell lung cancer cell lines compared with normal cell line. Paired box 2 was identified as a direct target for microRNA-744-5p in non-small cell lung cancer. Overexpression of microRNA-744-5p inhibits non-small cell lung cancer cell proliferation, colony formation, and cell invasion in vitro through targeting paired box 2. The present study provided novel insights into the biological functions of microRNA-744-5p in non-small cell lung cancer.

LncRNA MAFG-AS1 boosts the proliferation of lung adenocarcinoma cells via regulating miR-744-5p/MAFG axis.

Lung adenocarcinoma (LUAD) is typically featured by a low 5-year survival rate, hence there is a necessary to investigate new biomarkers in LUAD progression. Competing endogenous RNA (ceRNA) network has been widely reported in the regulation of tumor processes, which is also the main direction of this paper. Based on the data of GEPIA database, lncRNA MAFG-AS1 was upregulated in LUAD tissues, which was associated with poor prognosis of patients. Proliferation or apoptosis of LUAD cells were measured by CCK-8, EdU and caspase-3 activity assays followed by Western blot. The results indicated that silencing of MAFG-AS1 suppressed cell proliferation but induced cell apoptosis. RNA FISH staining showing the cytoplasmic localization of MAFG-AS1 in LUAD cells. Mechanism detection revealed that MAFG-AS1 served as a molecular sponge of miR-744-5p to upregulate its nearby gene MAF bZIP transcription factor G (MAFG) in LUAD cells. Functionally, MAFG overexpression attenuated the cellular processes mediated by MAFG-AS1 knockdown. In summary, this study unveiled the MAFG-AS1/miR-744-5p/MAFG axis in LUAD, providing a potent and promising therapeutic target for LUAD patients.