MicroRNA-135b promotes proliferation, invasion and migration of osteosarcoma cells by degrading myocardin

Xu, Weiguo; Shang, Ying-Lie; Cong, Xian-Rui; Bian, Xia; Yuan, Zhen

doi:10.3892/ijo.2014.2641

Cited by 20 publications

(15 citation statements)

References 26 publications

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“…Similarly, various miRNAs were demonstrated to inhibit migration and invasion of OS cells by regulating various genes, including miR‐15 which targeted TNFAIP1 , miR‐218 which inhibited expressions of TIAM1 , MMP‐2 , and MMP‐9 and miR‐335 which regulated ROCK1 . On the contrary, many studies elucidated the role of miRNAs to promote OS cell invasion and migration, for instance, miR‐23a enhanced migration and invasion through PTEN in OS , miR‐135b promoted viability and mobility of OS cells by degrading myocardin and TGF‐β1 promoted osteosarcoma cell migration and invasion through the miR‐143‐versican pathway . However, our research expounded the down‐regulation of miR‐127‐3p in inhibiting OS cell invasion and migration.…”

Section: Discussionmentioning

confidence: 99%

MiR‐127‐3p inhibits cell growth and invasiveness by targeting ITGA6 in human osteosarcoma

Wang

Tang

et al. 2018

IUBMB Life

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Osteosarcoma (OS) is one of the most universal malignant bone tumors that occur mostly in children and adolescents. This study aimed to investigate the roles of miR-127-3p and integrin subunit-α 6 (ITGA6) in OS proliferation, apoptosis, invasion and migration, and to explore the possible molecular mechanism and target relationship. By conducting quantitative real-time polymerase chain reaction (qRT-PCR) and western blot, the microRNA (miRNA) and protein expressions of miR-127-3p and ITGA6 in both tissues and cells were determined. The expression of apoptosis and migration related were also detected by western blot. The target relationship between miR-127-3p and ITGA6 was predicted by TargetScan and verified by dual-luciferase reporter assay. The biological functions of miR-127-3p and ITGA6 in OS were investigated by following experiments: cell counting kit 8 (CCK-8) and colony formation assays to inspect cell proliferation, flow cytometry, and caspase 3 activity assay to examine apoptosis, and transwell and wound healing assays to analyze invasion and migration. Significant down-regulation of miR-127-3p and up-regulation of ITGA6 was found out in OS tissues and cells. ITGA6 was proved to be the downstream target gene of miR-127-3p and functioned as a tumor promotor in OS, while miR-127-3p restrained deterioration of OS by suppressing cell viability, reducing migration and invasion, and promoting apoptosis. MiR-127-3p suppressed proliferation, invasion, and migration while stimulated apoptosis of OS cells through knocking down ITGA6. © 2018 IUBMB Life, 70(5):411-419, 2018.

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Section: Discussionmentioning

confidence: 99%

MiR‐127‐3p inhibits cell growth and invasiveness by targeting ITGA6 in human osteosarcoma

Wang

Tang

et al. 2018

IUBMB Life

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“…This post-transcriptional process of MYOCD regulation could explain why there is only transient expression of many SMC-restricted genes in the embryonic heart, only to re-emerge in adult hearts undergoing failure. There are other miR-binding sites in the MYOCD 3′ un-translated region including miR-9[64] and miR-135b[93] that effect changes in cardiac hypertrophy and cellular growth, respectively. It will be important to define the dynamic interplay among the known and yet-to-be-defined microRNAs that bind and regulate MYOCD expression.…”

Section: Regulatory Control Of Myocardin Expression and Activitymentioning

confidence: 99%

Myocardin in biology and disease

Miano

2015

J Biomed Res

100

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Myocardin (MYOCD) is a potent transcriptional coactivator that functions primarily in cardiac muscle and smooth muscle through direct contacts with serum response factor (SRF) over cis elements known as CArG boxes found near a number of genes encoding for contractile, ion channel, cytoskeletal, and calcium handling proteins. Since its discovery more than 10 years ago, new insights have been obtained regarding the diverse isoforms of MYOCD expressed in cells as well as the regulation of MYOCD expression and activity through transcriptional, post-transcriptional, and post-translational processes. Curiously, there are a number of functions associated with MYOCD that appear to be independent of contractile gene expression and the CArG-SRF nucleoprotein complex. Further, perturbations in MYOCD gene expression are associated with an increasing number of diseases including heart failure, cancer, acute vessel disease, and diabetes. This review summarizes the various biological and pathological processes associated with MYOCD and offers perspectives to several challenges and future directions for further study of this formidable transcriptional coactivator.

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“…Although their importance in mammary myoepithelial differentiation (14,15) and the epithelial-mesenchymal transition (EMT) (16) has been established, their functions in cancer are completely different between myocardin and MRTF-A/B. Myocardin as an effective inducer of growth arrest and differentiation of certain tumors and is frequently repressed during human malignant transformation (12,17). Yet, MRTF-A/B promotes tumor cell invasion and metastasis (18).…”

Section: Introductionmentioning

confidence: 99%

The MRTF-A/B function as oncogenes in pancreatic cancer

et al. 2015

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Despite evidence that MRTF-A/B, co-activators of serum response factor (SRF), promotes tumor cell invasion and metastasis in cancer, there are no studies describing MRTF-A/B in pancreatic cancer. To clarify involvement of MRTF-A/B expression in pancreatic cancer, we used quantitative reverse transcription-polymerase chain reaction and western blot analysis to detect MRTF-A/B in pancreatic cancer, intraductal papillary mucinous neoplasm (IPMN) and non-neoplastic pancreata. MRTF-A/B expression differs significantly between cancer and non-neoplastic tissues as well as between non-neoplastic tissues and IPMN bulk tissues. Next, we studied the roles of MRTF-A/B in vitro. Overexpression of MRTF-A/B promoted epithelial-mesenchymal transition (EMT) and generated stem cell-like cells in normal pancreatic cells. We performed quantitative reverse transcription-polymerase chain reaction to detect the level of MRTF-A/B in 19 pancreatic cancer cell lines. We found that their expression was associated with gemcitabine resistance. Like in normal pancreatic cells, MRTF-A/B also promoted EMT and promoted formation of stem cell-like cells in pancreatic cancer and they could regulate microRNA expression associated with EMT and CICs. Finally, to further demonstrate the roles of MRTF-A/B in vivo, we performed nude mouse model of s.c. xenograft and found that overexpression of MRTF-A and MRTF-B promoted pancreatic cancer growth. Elucidating the roles of MRTF-A/B will help us to further understand molecular basis of the disease and offer new gene targets for effective therapies.

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MicroRNA-135b promotes proliferation, invasion and migration of osteosarcoma cells by degrading myocardin

Cited by 20 publications

References 26 publications

MiR‐127‐3p inhibits cell growth and invasiveness by targeting ITGA6 in human osteosarcoma

MiR‐127‐3p inhibits cell growth and invasiveness by targeting ITGA6 in human osteosarcoma

Myocardin in biology and disease

The MRTF-A/B function as oncogenes in pancreatic cancer

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