MicroRNA-10a targets CHL1 and promotes cell growth, migration and invasion in human cervical cancer cells

Long, Meijing; Wu, Fuxia; Li, Pu; Liu, Min; Li, Xin; Tang, Hua

doi:10.1016/j.canlet.2012.05.022

Cited by 131 publications

(98 citation statements)

References 52 publications

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“…The target mRNAs of miRNAs are being uncovered, including the verified targets for miR-10a, such as fms-related tyrosine kinase 1,27) cell adhesion molecule L1-like, 28) phosphatase and tensin homolog, 29) and EPH receptor A8 30) in some diseases. More importantly, miR-10a is found to repress TBX5 protein levels by targeting TBX5 3'UTR.…”

Section: Discussionmentioning

confidence: 99%

microRNA-10a Targets T-box 5 to Inhibit the Development of Cardiac Hypertrophy

Wang

Zhai

et al. 2017

Int. Heart J.

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SummaryThe mechanism of cardiac hypertrophy involving microRNAs (miRNAs) is attracting increasing attention. Our study aimed to investigate the role of miR-10a in cardiac hypertrophy development and the underlying regulatory mechanism.Transverse abdominal aortic constriction (TAAC) surgery was performed to establish a cardiac hypertrophy rat model, and angiotensin II (AngII) was used to induce cardiac hypertrophy in cultured neonatal rat cardiomyocytes. Expression of T-box 5 (TBX5) and miR-10a was altered by cell transfection of siRNA or miRNA mimic/inhibitor. Leucine incorporation assay, histological and cytological examination, quantitative real-time PCR (qRT-PCR), and Western blot were performed to detect the effects of miR-10a and TBX5 on cardiac hypertrophy. Dual-luciferase reporter assay was conducted to verify the regulation of TBX5 by miR-10a.miR-10a was down-regulated, and TBX5 was up-regulated in the rat model and AngII-stimulated cardiomyocytes. miR-10a inhibited TBX5 expression by directly targeting the binding site in Tbx5 3'UTR. Overexpression of miR-10a in AngII-treated cardiomyocytes decreased relative cell area, and significantly reduced the mRNA levels of natriuretic peptide A (Nppa), myosin heavy chain 7 cardiac muscle beta (Myh7), and leucine incorporation (P < 0.01 or P < 0.001). Knockdown of Tbx5 had similar effects on AngII-induced cardiomyocytes.Our findings indicate that miR-10a may inhibit cardiac hypertrophy via targeting Tbx5. Thus, miR-10a provides promising therapeutic strategies for the treatment of cardiac hypertrophy. (Int Heart J 2017; 58: 100-106)

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Section: Discussionmentioning

confidence: 99%

microRNA-10a Targets T-box 5 to Inhibit the Development of Cardiac Hypertrophy

Wang

Zhai

et al. 2017

Int. Heart J.

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“…Recently, the role of microRNAs (miRNAs), 2 a class of small RNAs that post-transcriptionally regulate target gene expression in a sequence-specific manner, has received widespread attention (3,4). The dysregulation of miRNAs affects many aspects of cervical cancer, including cellular apoptosis, cell cycle progression, and cell migration and invasion (5)(6)(7). miRNAs are transcribed as long primary transcripts that are subsequently processed by the RNase III proteins Drosha and Dicer to form mature microRNAs (8).…”

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confidence: 99%

miR-346 Up-regulates Argonaute 2 (AGO2) Protein Expression to Augment the Activity of Other MicroRNAs (miRNAs) and Contributes to Cervical Cancer Cell Malignancy

Guo

Liu

et al. 2015

Journal of Biological Chemistry

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MicroRNAs (miRNAs) are a class of post-transcriptional regulators of gene expression, and AGO2 is essential for miRNA activity. In this study, we focused on the regulation of AGO2 by miR-346 and the consequences in cervical cancer cells. miR-346 enhanced the expression of AGO2, resulting in the increased activity of other miRNAs and contributing to the malignancy of HeLa cells. GRSF1 participated in the regulation of AGO2 by miR-346, and the middle sequence of miR-346 was vital for the synergy effect of miR-346 and GRSF1. We determined that miR-346 promoted the migration and invasion of HeLa cells. In summary, we are the first to report that AGO2 is regulated positively by miRNA and that GRSF1 participates in the miRNA pathway.Cervical cancer is one of the most prevalent gynecological cancers worldwide, accounting for ϳ12% of all cancers globally (1). The etiology of cervical cancer varies, and high-risk human papilloma virus infection is one of the most prominent features of cervical cancer (2). Recently, the role of microRNAs (miRNAs), 2 a class of small RNAs that post-transcriptionally regulate target gene expression in a sequence-specific manner, has received widespread attention (3, 4). The dysregulation of miRNAs affects many aspects of cervical cancer, including cellular apoptosis, cell cycle progression, and cell migration and invasion (5-7). miRNAs are transcribed as long primary transcripts that are subsequently processed by the RNase III proteins Drosha and Dicer to form mature microRNAs (8). Then, a strand of mature miRNA is incorporated into an RNA-induced silencing complex (RISC), where it exerts its effects. AGO2 is a key component of the RISC and is the only AGO2 protein with intrinsic endonuclease activity (9). The expression of AGO2 is tightly regulated at both transcriptional and post-transcriptional levels (10). Dysregulation of AGO2 has been reported in many tumors, including lung cancer (11), prostate cancer (12, 13), hepatocarcinoma (14), and melanoma (15), but the role of AGO2 and how its expression is regulated in cervical cancer have not been well studied.In this study, we found that AGO2 was expressed in cervical cancers and that its expression was enhanced by miR-346 and GRSF1 independent of an increase in AGO2 stability. The increased expression of AGO2 augmented the activity of other miRNAs and promoted the malignant phenotype of cervical cancer cells. These findings could provide new insights into the regulation of AGO2 expression and the mechanisms by which miRNAs up-regulate the expression of their target genes. Materials and Methods Cell Lines and Clinical Tissue Samples-The cancer cell lines used in this study were preserved in liquid nitrogen in our laboratory, and the cells were maintained in standard culture medium as recommended by the ATCC. All transfections were performed with Lipofectamine TM 2000 reagent (Invitrogen) according to the recommendations of the manufacturer. Fourteen pairs of clinical cervical cancer tissues and respective adjacent non-cancerous tissues were...

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“…In particular, 12 of the 31 identified genes have been reported in the literatures to be related to colon cancer recurrence [23][24][25][26][27][28][29][30][31][32][33][34][35][36][37], which can be regarded as validation to our prediction results for these 12 genes. For the other 19 genes identified by us, we cannot exclude the possibility that some of them are due to false positive prediction.…”

Section: Discussionmentioning

confidence: 54%

Exploration of immunogene in colon cancer recurrence

Sun¹,

Yao²,

Yuan³

et al. 2018

Oncotarget

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Colon adenocarcinoma is the third most common cancer with high risk of recurrence and deteriorative consequences. Given the importance of immune genes in tumor regulation and cancer immunotherapy, there is a need to comprehensively profile the immunoregulatory genes from multiple types of colon cancer patient genomic data for discovering important associations and potential therapeutic targets of colon cancer recurrence. We used publicly available colon tumor tissue genomic data from The Cancer Genome Atlas database and immune genes data from innateDB database in this study. We derived the immune genes profiles by exploring multiple genomic profiles (gene expression, clinical and somatic mutation) in colon cancer. Some of the synthetic lethal genes we identified, such as CASP14, MS4A6E, KIR2DL1, KIR3DL1, KIR2DL3, CCL1, IL36B, FOXO3, POU2F1, SMAD3, HOXA9, PACS1, PROM1, DIDO1, SRC, CBFA2T2, NCOA6, PGAM1 and PROC, have been suggested to be potential targets correlated with immune genes for colon cancer recurrence treatment. Moreover, TLR2 could be promisingly new early stage indicator for colon adenocarcinoma recurrence. This is a systematic study that combines three different types of genomic data to molecularly characterize colon cancer and aims to identify potential targets for colon adenocarcinoma therapy. Meanwhile, the integrative analysis of immune genes for colon cancer could assist in identifying potential new symbols for colon adenocarcinoma recurrence.

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MicroRNA-10a targets CHL1 and promotes cell growth, migration and invasion in human cervical cancer cells

Cited by 131 publications

References 52 publications

microRNA-10a Targets T-box 5 to Inhibit the Development of Cardiac Hypertrophy

microRNA-10a Targets T-box 5 to Inhibit the Development of Cardiac Hypertrophy

miR-346 Up-regulates Argonaute 2 (AGO2) Protein Expression to Augment the Activity of Other MicroRNAs (miRNAs) and Contributes to Cervical Cancer Cell Malignancy

Exploration of immunogene in colon cancer recurrence

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