Hsa-miR-19a is associated with lymph metastasis and mediates the TNF-α induced epithelial-to-mesenchymal transition in colorectal cancer

Huang, Likun; Wang, Xiaoyan; Wen, Chuangyu; Yang, Xiangling; Song, Minmin; Chen, Junxiong; Wang, Chenliang; Zhang, Bo; Wang, Lei; Iwamoto, Aikichi; Wang, Jianping; Liu, Huanliang

doi:10.1038/srep13350

Cited by 74 publications

(62 citation statements)

References 39 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This argues that miR-19a regulation has functional effects, although its regulation by PLEKHA7 is probably indirect. Interestingly, a recent report has indicated the involvement of miR-19a in colon tumorigenesis, 42 which is consistent with our findings in the colonic Caco2 cells. Together, the data further support the anti-tumorigenic role of PLEKHA7, via regulation of miRNA expression at multiple levels.…”

Section: Plekha7 Maintains the Integrity Of The Apical Cortical Actinsupporting

confidence: 93%

PLEKHA7 defines an apical junctional complex with cytoskeletal associations and miRNA-mediated growth implications

Kourtidis

Anastasiadis

2016

Cell Cycle

View full text Add to dashboard Cite

E-cadherin-p120 catenin complexes are essential for adherens junction (AJ) formation and for the maintenance of the normal epithelial phenotype. PLEKHA7 was originally identified as a member of this complex that tethers microtubules to the AJs and supports their overall integrity. Recently, we revealed that PLEKHA7 regulates cellular behavior via miRNAs by associating with the microprocessor complex at the apical zonula adherens (ZA). We have also identified a new set of PLEKHA7 interacting partners at the apical ZA, via proteomics. Our analysis shows that the main groups of proteins associating with PLEKHA7 are cytoskeletal-related and RNA-binding proteins. Here, we provide extended evidence for association of PLEKHA7 with several of these proteins. We also show that PLEKHA7 loss activates the actin regulator cofilin in a p120-dependent manner, providing an explanation for the effects of PLEKHA7 on the cortical actin ring. Interestingly, PLEKHA7 regulates the levels and associates with PP1α, a phosphatase responsible for cofilin activation. Finally, we clarify the mode of regulation of the oncogenic miR-19a by PLEKHA7. Overall, our findings support a multi-layered role of PLEKHA7 in converging cytoskeletal dynamics and miRNA-mediated growth regulation at the ZA, with potentially critical implications in cancer that warrant further investigation.

show abstract

Section: Plekha7 Maintains the Integrity Of The Apical Cortical Actinsupporting

confidence: 93%

PLEKHA7 defines an apical junctional complex with cytoskeletal associations and miRNA-mediated growth implications

Kourtidis

Anastasiadis

2016

Cell Cycle

View full text Add to dashboard Cite

show abstract

“…26 Tumor necrosis factor-α (TNF-α) upregulated the expression of miR-19a, and the miR-19a was required for TNF-α-induced epithelial-to-mesenchymal transition (EMT) and metastasis in colorectal cancer cells. 27 For lung cancer patients, high levels of miR-19a were associated with poor prognosis of lung cancer. MiR-19a promoted proliferation and metastasis of lung cancer cells by targeting MAX dimerization protein 1 (MXD1).…”

Section: Discussionmentioning

confidence: 99%

MiR-19a regulates the cell growth and apoptosis of osteosarcoma stem cells by targeting PTEN

et al. 2017

View full text Add to dashboard Cite

MicroRNAs are small, endogenous, and non-coding RNAs that play important regulatory roles in multiple biological processes in cancers. Recent evidence has indicated that miR-19a participates in the cancer tumorigenic progression. However, the functional roles of miR-19a in cancer stem cells are still unclear. As the cancer stem cells are considered to be responsible for the tumor recurrence and treatment failure in osteosarcoma, the aim of this study is to investigate the molecular mechanism of miR-19a underlying osteosarcoma tumorigenesis. In this study, we observed significant upregulation of miR-19a in osteosarcoma patients' tumor tissues as well as the osteosarcoma cell lines in vitro. We showed that knockdown of miR-19a by its antisense oligonucleotide (anti-miR-19a) significantly decreased the population of cancer stem cells in osteosarcoma cell lines. Furthermore, we found the miR-19a regulated the cell proliferation, migration, and viability in the human osteosarcoma-cancer stem cells. The gene of phosphatase and tensin homolog deleted on chromosome 10, which is an important tumor suppressor, was found to be directly regulated by miR-19a in human osteosarcoma-cancer stem cells. We demonstrated that knockdown of miR-19a increased the expression of phosphatase and tensin homolog deleted on chromosome 10. As the anti-miR-19a inhibited the phosphatidylinositol 3-kinase/AKT pathway and induced apoptosis of human osteosarcoma-cancer stem cells, the phosphatase and tensin homolog deleted on chromosome 10 small interfering RNA inhibited the effect of it. Meanwhile, the phosphatase and tensin homolog deleted on chromosome 10 small interfering RNA also abolished the effect of anti-miR-19a on inhibiting the cell proliferation, migration, and viability in the human osteosarcoma-cancer stem cells. In conclusion, our findings demonstrated that dysregulation of miR-19a plays critical roles in the osteosarcoma stem cells, at least in part via targeting the phosphatase and tensin homolog deleted on chromosome 10. Knockdown of miR-19a may represent a potential strategy for the osteosarcoma treatment.

show abstract

“…High levels of miR-18a in CRC have been revealed to attenuate the repair function of DNA and induce carcinogenesis by targeting ATM to suppress ATM expression (12). The overexpression of miR-19a in CRC cells has been indicated to promote cell invasion and the epithelial-mesenchymal transition (EMT), and has been revealed to be associated with lymph node metastasis (37). In a previous study, miR-92a upregulated β-catenin and vimentin, and downregulated epithelial-cadherin, targeting PTEN induced EMT in CRC through the PTEN/phosphoinositide 3 kinase/protein kinase B pathway (22).…”

Section: Function and Mechanisms Of Microrna-20a In Colorectal Cancermentioning

confidence: 99%

Function and mechanisms of microRNA‑20a in colorectal cancer (Review)

et al. 2020

View full text Add to dashboard Cite

Colorectal cancer (CRC) is the third most common malignancy and the second leading cause of cancer-associated mortality worldwide. CRC currently has no specific biomarkers to promote its diagnosis and treatment and the underlying mechanisms regulating its pathogenesis have not yet been determined. MicroRNAs (miRs) are small, non-coding RNAs that exhibit regulatory functions and have been demonstrated to serve a crucial role in the post-transcriptional regulatory processes of gene expression that is associated with cell physiology and disease progression. Recently, abnormal miR-20a expression has been identified in a number of cancers types and this has become a novel focus within cancer research. High levels of miR-20a expression have been identified in CRC tissues, serum and plasma. In a recent study, miR-20a was indicated to be present in feces and to exhibit a high sensitivity to CRC. Therefore, miR-20a may be used as a marker for CRC and an indicator that can prevent the invasive examination of patients with this disease. Changes in the expression of miR-20a during chemotherapy can be used as a biomarker for monitoring resistance to treatment. In conclusion, miR-20a exhibits the potential for clinical application as a novel diagnostic biomarker and therapeutic target for use in patients with CRC. The present study focused on the role and mechanisms of miR-20a in CRC. Contents 1. Introduction 2. microRNA-20a overview 3. The mechanism of miR-20a in CRC 4. miR-20a can be used as a diagnostic marker in CRC 5. miR-20a may be used as a monitoring indicator during chemotherapy 6. Conclusion and prospects

show abstract

Hsa-miR-19a is associated with lymph metastasis and mediates the TNF-α induced epithelial-to-mesenchymal transition in colorectal cancer

Cited by 74 publications

References 39 publications

PLEKHA7 defines an apical junctional complex with cytoskeletal associations and miRNA-mediated growth implications

PLEKHA7 defines an apical junctional complex with cytoskeletal associations and miRNA-mediated growth implications

MiR-19a regulates the cell growth and apoptosis of osteosarcoma stem cells by targeting PTEN

Function and mechanisms of microRNA‑20a in colorectal cancer (Review)

Contact Info

Product

Resources

About