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Search indexed NASA NTRS and DOE OSTI research on propulsion, heat transfer, battery materials and energy systems. Follow report and document links to the original sources.

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At least 271 records · Page 15
All sourcesNASA NTRSDOE OSTI
DOE OSTI2017

Increased expression of microRNA-31-5p inhibits cell proliferation, migration, and invasion via regulating Sp1 transcription factor in HepG2 hepatocellular carcinoma cell line

Accumulating evidence has suggested that microRNA-31-5p (miR-31-5p) is dysfunctional in hepatocellular carcinoma (HCC). However, the molecular mechanism of HCC remains unclear. In this study, we investigated the role of miR-31-5p in tumor formation and development of HCC. The expression of miR-31-5p was detected in HCC tissues, corresponding adjacent tissues, normal liver tissues, and HCC cell lines. miR-31-5p mimics and an inhibitor were transfected into HepG2 cells to assess the effects of miR-31-5p on cell proliferation, apoptosis, cell cycle, migration, and invasion assays. Western blotting was used to detect the expression of Sp1 transcription factor (SP1), cyclin D1, and survivin in transfected HCC cells and control cells. The expression of miR-31-5p was significantly decreased in HCC cells and HCC tissues. Overexpression of miR-31-5p inhibited HCC cell growth, migration, and invasion. Overexpression of miR-31-5p reduced the expression of SP1 and cyclin D1, and knockdown of SP1 decreased cyclin D1 expression. The dual luciferase assay showed that miR-31-5p directly targeted SP1 in HepG2. Together, the results suggested that miR-31-5p acted as a tumor suppressor to regulate SP1, and that miR-31-5p could be used as a therapeutic target for the treatment of HCC. - Highlights: • The expression of miR-31-5p was significantly up-regulated in HCC tissues. • Increased expression of miR-31-5p inhibits cell proliferation, migration, and invasion. • Sp1 transcription factor is the target gene for miR-31-5p.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

miR-455-3p serves as prognostic factor and regulates the proliferation and migration of non-small cell lung cancer through targeting HOXB5

MicroRNAs (miRs) have been reported to play significantly roles in the initiation and progression of human cancers. miR-455-3p has been recently found could function as tumor suppressor in various human cancers. However, its expression and biological role in non-small cell lung cancer (NSCLC) remains elusive. In this study, we found miR-455-3p was markedly downregulated in NSCLC tissues and cell lines. Chi-square test to analyze the correlations between miR-455-3p expression and clinicopathological features revealed that miR-455-3p expression was correlated with poorly differentiated cancer and advanced tumor stage (P P = 0.029). Univariate and multivariate analyses identified low miR-455-3p expression was an unfavorable prognostic factor for overall survival. Gain-of-function and loss-of-function studies revealed that miR-455-3p inhibits cell proliferation and migration in vitro. Computer algorithm and dual-luciferase reporter assay revealed that miR-455-3p directly targets and suppresses HOXB5 in NSCLC. Further studies demonstrated that knockdown of HOXB5 attenuated the effect of miR-455-3p downregulation on cell proliferation and migration. Taken together, our results for the first time suggested that miR-455-3p was downregulated in NSCLC and was correlated with the poor prognosis of NSCLC patients. Also, miR-455-3p functions as tumor suppressor by directly targeting HOXB5 in NSCLC progression and may be used as a potential target for NSCLC treatment.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

Long noncoding RNA SNHG15 promotes human breast cancer proliferation, migration and invasion by sponging miR-211-3p

Long non-coding RNAs (lncRNA) have been demonstrated to act as essential regulators in the development and progression of breast cancer. In our study, we found that long noncoding RNA SNHG15 was highly expressed in breast cancer tissues and cell lines. And the expression of SNHG15 was correlated with TNM stage, lymphnode metastasis and survival in breast cancer patients. SNHG15 knockdown significantly inhibited the proliferation and induced apoptosis in breast cancer cells in vitro and in vivo. Besides, SNHG15 downregulation suppressed cell migration and invasion in MCF-7 and BT-20 cells, and inhibited epithelial-mesenchymal transition (EMT). In mechanism, we found that SNHG15 acted as a competing endogenous RNA to sponge miR-211-3p, which was downregulated in breast cancers and inhibited cell proliferation and migration. Our results showed that there was a negative correlation between SNHG15 and miR-211-3p expression in breast cancer patients. Collectively, we, for the first time, revealed the functions of SNHG15 and miR-211-3p in breast cancer.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

High expression of diffuse panbronchiolitis critical region 1 gene promotes cell proliferation, migration and invasion in pancreatic ductal adenocarcinoma

Highlights: • DPCR1 is overexpressed in PDAC and correlates with prognosis of PDAC patients. • Inhibition of DPCR1 suppresses PDAC cell proliferation in vitro and in vivo. • Inhibition of DPCR1 suppresses PDAC cell migration and invasion. • DPCR1 may promote tumor progression by regulating NF-κB pathway. Diffuse panbronchiolitis critical region 1 (DPCR1) is located in the major histocompatibility complex (MHC) class I. It was reported to be downregulated in invasive pituitary adenoma compared with that in non-invasive tumors, but upregulated in the precursor of gastric carcinogenesis. However, the direct effect of DPCR1 on cancer cells has rarely been reported, and the role DPCR1 in pancreatic ductal adenocarcinoma (PDAC) remains unclear. The clinical sample validation and public data analysis of the present study demonstrated that DPCR1 was upregulated markedly in PDAC and this high expression was negatively correlated with the patient prognosis. Functionally, knocking down DPCR1 in PDAC cell lines inhibited cell proliferation, migration and invasion in vitro. Tumor xenograft experiments further showed that suppression of DPCR1 inhibited tumor growth in vivo. In addition, the results of RNA deep sequencing and qRT-PCR assay showed that DPCR1 participated in PADC progression by regulating nuclear factor-kappa B signaling pathway, suggesting that it might be a novel oncogene in tumor progression and a potential therapeutic target in PDAC as well.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

Zika virus infected primary microglia impairs NPCs proliferation and differentiation

Highlights: • ZIKV infects primary microglia and induce inflammatory response. • ZIKV infected microglia decreases NPCs proliferation. • ZIKV infected microglia promote astrogenesis at the expense of neurogenesis. • Cytokines secreted by ZIKV infected microglia decrease neurogenesis. Zika virus (ZIKV) can lead to severe birth defects especially microcephaly in newborns by infecting human neural progenitors and impairing brain development. However, as the resident immune cells in the brain, the role of microglia in the ZIKV pathology is not clearly defined. To understand the interplay between immune response and neural cells, we investigate the interaction between microglia and NPCs during ZIKV infection. Our results demonstrate that primary microglia infected with ZIKV induces an inflammatory response similar to that in human, producing high level of tumor necrosis factor alpha (TNF-α), interleukin 6 (IL-6), interleukin 1β (IL-1β) and inducible nitric oxide synthase (iNOS). Furthermore, conditional medium (CM) of ZIKV infected microglia showed inhibitory effects on cell proliferation and neuronal differentiation of neural precursor cells (NPCs) derived from E14 mice brain. Blocking cytokines in the CM remarkably improved neurogenesis and decreased astrocytic differentiation of NPCs. Together, our results suggest that microglia mediated neuroinflammation plays an important role in neuropathogenesis during ZIKV infection.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

LncRNA FABP5P3/miR-589-5p/ZMYND19 axis contributes to hepatocellular carcinoma cell proliferation, migration and invasion

Hepatocellular carcinoma (HCC) contributes to cancer-related deaths greatly every year in the world. However, there is still no radical method for HCC treatment. Here we screened out a lncRNA FABP5P3 that was up-regulated in HCC tissues. Patients with higher FABP5P3 expression displayed poorer survival rate. FABP5P3 depletion in HCC cell lines and sample cells remarkably inhibited the abilities of proliferation, migration and invasion. In mechanism, we showed that FABP5P3 bond to miR-589-5p which served as a tumor suppressor. MiR-589-5p targeted directly the mRNA of ZMYND19 whose function has not been defined in HCC. FABP5P3 promoted HCC development and progression by sponging miR-589-5p and up-regulating ZMYND19 expression. In sum, we showed that FABP5P3/miR-589-5p/ZMYND19 axis regulates cell proliferation and migration in HCC, which may serve as a new target for HCC treatment.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

MicroRNA-585 suppresses tumor proliferation and migration in gastric cancer by directly targeting MAPK1

Highlights: • MiR-585 is down-regulated in gastric cancer tissues. • Down-regulation of miR-585 indicates poor prognosis for GC patients. • MiR-585 inhibits GC cell proliferation and migration by targeting MAPK1. Increasing evidence reveals that microRNA contributes to the development and progression of gastric cancer (GC), but the roles of miR-585 in GC remain unclear. In this study, we confirmed that miR-585 was down-regulated in GC tissues and cell lines and that miR-585 expression was related to extent of invasion, TNM stage, lymph node invasion and poor prognosis. Our results showed that miR-585 inhibits the proliferation and migration of GC, and MAPK1 is a direct and functional target of miR-585. Our study sheds light on the role of miR-585 as a suppressor for tumor growth and metastasis and raises the intriguing possibility that miR-585 may serve as a new potential marker for monitoring and treating GC.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

Long noncoding RNA LNC473 inhibits the ubiquitination of survivin via association with USP9X and enhances cell proliferation and invasion in hepatocellular carcinoma cells

Highlights: • LNC473 was overexpressed in HCC tissues and correlated with tumor size, BCLC stage, vascular invasion and poor prognosis. • LNC473 enhanced HCC cell proliferation and invasion and induced epithelial–mesenchymal transition (EMT) process. • LNC473 associated with oncoprotein survivin and regulates its stability. • LNC473 recruited USP9X to inhibit survivin ubiquitination and then increase its expression. Hepatocellular carcinoma (HCC) is the third leading cause of cancer-related death worldwide. Recent studies reported that lncRNA LINC00473 (LNC473) was involved in cancer progression. However, the clinical significance and functional role of LNC473 in HCC progression is still unknown. In the present study, we found that the LNC473 expression was markedly elevated in HCC tissues and correlated with bigger tumor size, higher BCLC stage, vascular invasion and poor prognosis. Gain- and loss-of-function assay showed that LNC473 enhanced HCC cell proliferation and invasion and induced epithelial–mesenchymal transition (EMT) process. Mechanistically, LNC473 associated with oncoprotein survivin and regulates its stability. Moreover, LNC473 could recruit deubiquitinase USP9X to inhibit the ubiquitination level of survivin and then increase survivin expression. Therefore, our results suggest that LNC473 exerts its functions as an oncogene in HCC progression and may be a therapeutic target for HCC treatment.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

MiR-615 inhibits cell proliferation, migration and invasion by targeting EGFR in human glioblastoma

Highlights: • MiR-615 is decreased in GBM. • MiR-615 is a tumor suppressor. • MiR-615 targets EGFR 3′-UTR. MiR-615 and epidermal growth factor receptor (EGFR) are associated with a number of disease processes and pathogenesis. However, little is known about the mechanisms of miR-615 and EGFR in human glioblastoma multiforme (GBM). Here, we found that down-regulation of miR-615 expression occurred in GBM tissues and cells, and was inversely correlated with overall survival, relapse-free survival, WHO grade as well as EGFR expression. We further determined that miR-615 functions as a tumor suppressor by inhibiting GBM cell proliferation, cell cycle, migration and invasion, and promoting cell apoptosis. In-vivo assay validated the inhibition effect of miR-615 on tumor growth and EGFR expression. Luciferase reporter assays demonstrated that miR-615 targeted the 3′-untranslated region (3′-UTR) of EGFR. Besides, over-expression of EGFR reversed the inhibition effects of miR-615, while silencing of EGFR aggravated these inhibition effects. In conclusions, we identified that miR-615 plays a tumor suppressor role in GBM cell proliferation, migration and invasion by targeting EGFR expression, and miR-615 may act as a novel biomarker for early diagnosis or therapeutic targets of GBM.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

Knockout of NCOA5 impairs proliferation and migration of hepatocellular carcinoma cells by suppressing epithelial-to-mesenchymal transition

Highlights: • Generation of NCOA5-knockout HCC cell lines using CRISPR/Cas9. • Knockout of NCOA5 inhibits the proliferation and migration of HCC cells. • Knockout of NCOA5 depresses the tumor microsphere formation of HCC cells. • Knockout of NCOA5 suppresses EMT. Nuclear receptor coactivator 5 (NCOA5) plays important roles in the development of a variety of malignancies. However, the underlying mechanisms remain obscure. In this study, we successfully generated the NCOA5 knockout hepatocellular carcinoma (HCC) cells by CRISPR/Cas9 - mediated genome editing and found that knockout of NCOA5 inhibited the proliferation and tumor microsphere formation of HCC cells significantly. Moreover, the migration ability of NCOA5 knockout HCC cells declined. Mechanistic analyses indicated that knockout of NCOA5 can suppress the epithelial - mesenchymal transition (EMT) in HCC cells. In conclusion, our findings provide a mechanistic insight into the role of NCOA5 in HCC progression.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

PBX1 promotes the cell proliferation via JAK2/STAT3 signaling in clear cell renal carcinoma

Highlights: • PBX1 is significantly upregulated in ccRCC tissues and cells, and associated with the overall survival in patients with ccRCC. • PBX1 mediates cell proliferation via JAK2/STAT3 signaling in ccRCC. • PBX1 acts as an oncogene in ccRCC by regulating the activation of JAK2/STAT3 signaling. PBX1 was abnormally overexpressed and its intracellular localization was found to be frequently amplified in many types of cancer, including renal clear cell carcinoma. PBX1 displays oncogenic activity in several different types of cells, but little is known about how signaling pathways are altered, and the function of PBX1 in renal clear cell carcinoma has not been well investigated. In this study, we demonstrate that the expression of PBX1 was significantly upregulated in 30 pairs of human tissues compared to adjacent normal tissues and the overall survival rate of PBX1-high group was significantly worse than that of PBX1-low group. Furthermore, JAK2 expression is significantly correlated to PBX1 expression in human clinical specimen and PBX1 knockdown inhibits STAT3 phosphorylation and reduced transcription of STAT3 target genes Cyclin D1. More interestingly, PBX1 knockdown inhibits ccRCC cell viability, proliferation and cell cycle progression in vivo and in vitro. Thus, our results demonstrate that PBX1 plays an oncogenic role in ccRCC via JAK2/STAT3 pathway and indicate its potential application for the treatment of human ccRCC in future.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

Apolipoprotein M promotes proliferation and invasion in non-small cell lung cancers via upregulating S1PR1 and activating the ERK1/2 and PI3K/AKT signaling pathways

Highlights: • ApoM was increased in NSCLC tissues and negatively correlated to preoperative CRP. • Enhanced ApoM expression could promote NSCLC proliferation, invasion and tumor growth. • It might be via upregulating S1PR1 and activating the ERK1/2, PI3K/AKT pathways. • Increased ApoM may relate to tumor microenvironment and local inflammation. Apolipoprotein M (ApoM) is a sphingosine 1-phosphate (S1P) carrier involved in the regulation of S1P. Signaling pathways involving sphingosine kinases (SphKs) and S1P-S1P receptors (S1PRs) play important roles in the oncogenesis of multiple cancers including non-small cell lung cancer (NSCLC). In the present study we have clarified the potential roles of ApoM on the oncogenesis process of NSCLC cells. We detected the ApoM expression in NSCLC tissues and further analyzed its clinical significance. Moreover, we determined effects of ApoM overexpression on tumor cellular behaviours of NSCLC in vitro and in vivo. Our results demonstrated that ApoM protein mass were clearly higher in the NSCLC tissues than in non-NSCLS tissues. Overexpression of ApoM could promote NSCLC cell proliferation and invasion in vitro and tumor growth in vivo, which might be via upregulating S1PR1 and activating the ERK1/2 and PI3K/AKT signaling pathways. It is concluded that up-regulation of ApoM in NSCLC might be associated with the tumor induced inflammation and tumor microenvironment as well as promoting oncogenesis of NSCLC. Further study needs to elucidate the underlying mechanisms.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

Long non-coding RNA MIAT is estrogen-responsive and promotes estrogen-induced proliferation in ER-positive breast cancer cells

Highlights: • lncRNA MIAT was over-expressed in ER-positive breast cancer tissues and cells. • Breast cancer cell MIAT expression was estrogen-dependent. • lncRNA MIAT promoted breast cancer cell growth. • lncRNA MIAT was required for breast cancer cell cycle progression. Estrogen drives the development and progression of estrogen receptor (ER)-positive breast cancer. However, the detailed mechanism underlying ER-driven carcinogenesis remains unclear despite extensive studies. Previously reports indicated higher expression of long non-coding RNA (lncRNA) myocardial infarction associated transcript (MIAT) in ER-positive breast cancer tissues than in ER-negative tissues. However, the functional relevance of MIAT in ER-positive breast cancer tumorigenesis was poorly understood. Here, we investigated the role of lncRNA MIAT in ER-positive breast cancer cells. MIAT was over-expressed in ER-positive breast cancer tissues and ER-positive breast cancer cell line MCF-7. Activating estrogen signaling by diethylstilbestrol (DES) led to a dose- and time-dependent up-regulation of MIAT in MCF-7 cells that was dependent on ERα, as evidenced by ERα silencing and pharmacological inhibition using ER antagonist ICI 182780. Silencing MIAT decreased DES-induced MCF-7 cell proliferation while overexpressing MIAT increased MCF-7 cell proliferation. Further mechanistic study identified that MIAT was critical for G1 to S phase cell cycle transition. Taken together, these results suggest that lncRNA MIAT is an estrogen-inducible lncRNA and a key regulator in ER-positive breast cancer cell growth. MIAT could serve as a potential biomarker and promising therapeutic target for ER-positive breast cancer.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

Circular RNA circZFR contributes to papillary thyroid cancer cell proliferation and invasion by sponging miR-1261 and facilitating C8orf4 expression

In recent years, more and more circular RNAs (circRNAs) have been identified in multiple tissues and cells. Increasing evidences show circRNAs play important roles in human cancers. However, the role of circRNAs in papillary thyroid carcinoma (PTC) remains largely unknown. In this study, we identified a new circRNA circZFR that was significantly upregulated in PTC tissues compared to adjacent normal tissues. Furthermore, circZFR expression level was negatively correlated with clinical severity. We found that circZFR knockdown dramatically inhibited the proliferation, migration and invasion of PTC cells in vitro. Mechanistically, we found circZFR could promote C8orf4 expression via serving as a competing endogenous RNA (ceRNA) of miR-1261 in PTC cells. Rescue assays indicated that restoration of C8orf4 significantly attenuated the inhibitory effects of circZFR knockdown on PTC cell proliferation, migration and invasion. In summary, our findings demonstrated that circRNA circZFR exerted oncogenic roles via regulating miR-1261/C8orf4 axis in PTC, which suggested circZFR might be a potential therapeutic target.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

LRP4 promotes proliferation, migration, and invasion in papillary thyroid cancer

Dysregulation of cell proliferation and death is considered the foundation of the malignant biological characteristics of cancer. In this study, we conducted a comprehensive analysis of a massively parallel whole transcriptome resequencing of paired papillary thyroid cancer and normal thyroid tissues from 19 patients. In addition, we found that LRP4, a member of the low-density lipoprotein receptor-related protein family, is significantly overexpressed in thyroid carcinoma. We demonstrated through quantitative real-time polymerase chain reaction (qRT-PCR) that LRP4 is upregulated in papillary thyroid cancer (PTC) tissues. This observation was also consistent with data analyzed from The Cancer Genome Atlas (TCGA) cohort. Thus, the biological role of LRP4 in the thyroid cancer in the present study was investigated using the PTC cell lines TPC1, BCPAP and KTC-1. In these cell lines, the mRNA level of LRP4 was higher than normal thyroid cancer cell named HTORI3. In vitro experiments demonstrated that LRP4 downregulation significantly inhibited the colony formation, proliferation, migration, and invasion of the three PTC cell lines. Knockdown of LRP4 by small interfering RNA (siRNA) in those cell lines decreased the protein expression of N-cadherin, Enhancer of zeste homolog 2 (EZH2), and Zinc finger E-box-binding home-box 1 (ZEB1). Furthermore, LRP4 knockdown significantly reduced the levels of phosphorylated PI3K in the PTC cell lines. In conclusion, the present study indicated that LRP4 is a gene associated with PTC and might become a potential therapeutic target.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

Circular RNA HIPK3 regulates human lens epithelial cells proliferation and apoptosis by targeting the miR-193a/CRYAA axis

Highlights: • CircRNA sequencing reveals 26 up-regulated and 75 down-regulated circRNAs in ARC. • CircHIPK3 is down-regulated in all three subtypes of ARC. • CircHIPK3 knockdown affects the cellular function in primary cultured HLECs. • CircHIPK3 exerts its role via modulation of circHIPK3/miR-193a/CRYAA axis in HLECs. Circular RNAs (circRNAs) are a novel class of non-coding RNAs generated from back splicing. Accumulating evidence has demonstrated their vital regulation in several biological processes and ocular diseases. However, the role of circRNAs in age-related cataract (ARC), the leading cause of visual impairment worldwide, is still unknown. CircRNA sequencing reveals that 101 circRNAs are differentially expressed between the capsules of transparent and ARC lenses, including 75 down-regulated circRNAs and 26 up-regulated circRNAs transcripts. Eight of 10 differentially expressed circRNAs are further verified by quantitative RT-PCRs. One highly conserved circRNA, circHIPK3, is significantly down-regulated in all cortical, nuclear and posterior subcapsular subtypes of ARC. The silencing of circHIPK3, but not HIPK3 mRNA, significantly accelerates apoptosis development upon oxidative stress and decreases cell viability and proliferation in primary cultured human lens epithelial cells (HLECs). The expression of α-SMA and vimentin was downregulated, while the expression of E-cadherin and ZO-1was upregulated, suggesting the repression of epithelial-mesenchymal transition after circHIPK3 knockdown. CircHIPK3 silencing increases miR-193a expression. miR-193a regulates CRYAA expression by targeting the binding site within the 3′UTR. Moreover, miR-193a decreases the viability and proliferation, and increases the apoptosis of HLECs upon oxidative stress. This study suggests that circRNAs are the potential regulators in cataractogenesis. CircHIPK3 regulates HLECs function through miR-193a-mediated CRYAA expression. This finding would provide a novel insight into the pathogenesis of ARC.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

Runx1 promotes satellite cell proliferation during ischemia - Induced muscle regeneration

RUNX1 is a transcription factor that is not expressed in uninjured muscles, but can be detected in denervated muscles, suggesting a role of RUNX1 in muscle's response to injury. However, the role of RUNX1 in muscle's response to ischemia has not been reported. Our study showed that Runx1 is up regulated in skeletal muscle during ischemia reperfusion induced injury. Over-expression of Runx1 in C2C12 cells inhibits myogenic differentiation, but promotes proliferation of myoblasts. Consistent with these findings, we found that Runx1 expression was decreased in differentiated satellite cells. Our results indicate that Runx1 regulates muscle regeneration by promoting proliferation of satellite cells.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

MicroRNA-613 promotes colon cancer cell proliferation, invasion and migration by targeting ATOH1

The aim of the present study is to investigate the expression and function of miR-613 in colon cancer (CC) and illuminate the molecular mechanisms underlying miR-613-regulated CC progression. Our data demonstrated that miR-613 was upregulated in CC tissue samples (P = 0.009) and human CC cell lines (HCT-116 and Lovo; P = 0.001 and P = 0.003, respectively), which also promoted the proliferation, invasion and migration of CC cells (P < 0.05). The dual-luciferase reporter assay confirmed that Atonal homolog1 (ATOH1) was the target mRNA of miR-613. Rescue experiments showed that ATOH1 overexpression vector significantly reversed the stimulative effects of miR-613 mimic on the progression of HCT-116 and Lovo cells (P < 0.001). Positive ATOH1 expression in CC tissues was significantly associated with lower grade (χ2 = 3.592, P = 0.043), lower TNM stage (χ{sup 2} = 3.537, P = 0.048) and better overall survival (P=0.041). Jun N-terminal kinase 1 (JNK1) pathway and Mucin 2 (MUC2) were the potential downstream proteins of miR-613/ATOH1. miR-613 is an oncogene in CC and promotes the proliferation, invasion and migration of CC cells by targeting ATOH1 likely via activating JNK1 pathway and upregulating MUC2.

60 APPLIED LIFE SCIENCES↗