microRNA-23b suppresses epithelial-mesenchymal transition (EMT) and metastasis in hepatocellular carcinoma via targeting Pyk2

Cao, Jie; Liu, Jinkai; Jianyun, Long; Fu, Jing; Huang, Liang; Li, Jing; Liu, Caifeng; Zhang, Xianghua; Yan, Yiqun

doi:10.1016/j.biopha.2017.02.030

Cited by 37 publications

(31 citation statements)

References 28 publications

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“…MiR-23b-3p overexpression inhibits the proliferative capability of breast cancer cells [23,24], ovarian cancer cells [25], hepatocarcinoma cells [18], colorectal cancer cells [21], and endometrial cancer cells [26]. However, a study conducted by Wang et al yielded inconsistent results [27].…”

Section: Discussionmentioning

confidence: 76%

“…It has been demonstrated that miR-23b-3p is expressed at low levels in a variety of malignant tumors, including liver cancer [18], bladder cancer [19], cervical cancer [20], colorectal cancer [21], and prostate cancer [22]. Our preliminary experiments showed that PDAC tissues and cell lines also expressed low levels of miR-23b-3p.…”

Section: Discussionmentioning

confidence: 91%

“…Proline-rich tyrosine kinase 2 (Pyk2) is an important factor in EMT [36]. MiR-23b-3p regulates Pyk2 via its 3′UTR, thereby affecting the migration and invasion of hepatocarcinoma cells [18]. MiR-23b-3p binds to the 3′UTR of a number of cytoskeletal genes, such as LIM domain kinase 2, Rho guanine nucleotide exchange factor 6, cofilin 2, phosphoinositide 3-kinase regulatory subunit 3, and urokinase-plasminogen activator.…”

Section: Discussionmentioning

confidence: 99%

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Biological Effect and Mechanism of the miR-23b-3p/ANXA2 Axis in Pancreatic Ductal Adenocarcinoma

Wei

Dang

Feng

et al. 2018

Cell Physiol Biochem

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Background/Aims: Accumulating evidence strongly suggests that microRNAs (miRNAs) modulate the expression of known tumor suppressor genes and oncogenes. In the present study, we found that the proliferation and invasion ability of pancreatic ductal adenocarcinoma (PDAC) cells were significantly suppressed by the overexpression of miR-23b-3p. In addition, there are miR-23b-3p binding sites in annexin A2 (ANXA2). Here, we investigated whether miR-23b-3p had an impact on the progression and metastasis of PDAC by targeting ANXA2. Methods: Cell proliferation, migration, and invasion, and cell cycle assays were performed to explore the effect of miR-23b-3p on various malignant phenotypes of pancreatic cancer cells. The size of tumors was observed following miR-23b-3p overexpression in an in vivo chick chorioallantoic membrane assay. Dual-luciferase reporter, quantitative real-time PCR, western blot, and immunohistochemical analyses were used to validate the relationship between miR-23b-3p and ANXA2 in vitro. Results: We observed that miR-23b-3p could bind specifically to the 3′ untranslated region of ANXA2 and inhibit its expression. MiR-23b-3p overexpression downregulated the expression of ANXA2 mRNA in PDAC cells and limited the size of tumors or even prevented tumor formation. In addition, there was a negative correlation between miR-23b-3p expression and ANXA2 protein expression in clinical specimens. Conclusion: MiR-23b-3p inhibits the development and progression of PDAC by regulating ANXA2 directly.

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Section: Discussionmentioning

confidence: 76%

Section: Discussionmentioning

confidence: 91%

Section: Discussionmentioning

confidence: 99%

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Biological Effect and Mechanism of the miR-23b-3p/ANXA2 Axis in Pancreatic Ductal Adenocarcinoma

Wei

Dang

Feng

et al. 2018

Cell Physiol Biochem

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“…miRNAs usually act as oncogenes or tumor suppressors in lung carcinoma, including miR-23b, miR-221, miR-148b, miR-423 and many other miRNAs (32). miR-23b was reported to suppress cell proliferation, migration and inhibit EMT in ovarian, bladder, hepatocellular, and prostate cancer (15–17,19,28). However, the role of miR-23b in lung carcinoma has not been reported.…”

Section: Discussionmentioning

confidence: 99%

“…miR-23b, has been reported to have low expression and be involved in multiple tumors, such as ovarian, bladder hepatocellular and prostate cancers (15–18). In hepatocellular cancer, miR-23b downregulates the expression of urokinase, c-Met and suppresses the migration and epithelial-mesenchymal transition (EMT) (15,19). Similar results have been reported in experimental autoimmune encephalomyelitis, i.e., that miR-23b suppresses leukocyte migration and pathogenesis (20).…”

Section: Introductionmentioning

confidence: 99%

miR‑23b suppresses lung carcinoma cell proliferation through CCNG1

et al. 2018

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Lung carcinoma with high incidence rate could be divided into four subtypes, including small cell carcinoma, squamous cell carcinoma, adenocarcinoma and large cell carcinoma. miR-23b has been reported to have a low expression and play major roles in abundant tumors, however there is little research in lung carcinoma and hence the purpose of this study was to explore the impact of miR-23b in lung carcinoma. The RNA level of miR-23b and cyclin G1 (CCNG1) was measured by reverse transcription quantitative PCR. Luciferase activity reporter assay was used to verify that CCNG1 is a target of miR-23b. MTT and Transwell assays were utilized to test the functional studies of miR-23b in lung cancer cells. In lung carcinoma and lung cancer cells miR-23b expression is low compared with that in paracancerous tissues and normal lung cells. Low miR-23b expression inhibited lung cancer cell proliferation measured by MTT assay. We applied luciferase reporter to determine whether CCNG1 is a target of miR-23b and there was a negative correlation between them. Moreover, interference with CCNG1 reduced the cell proliferation ability, which partially reversed function of miR-23b. miR-23b inhibited cell proliferation of lung cancer by directly targeting CCNG1. It is suggested that miR-23b/CCNG1 axis may present a new target for the treatment of lung cancer.

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Molecular signatures in hepatocellular carcinoma: A step toward rationally designed cancer therapy

Erstad

Fuchs

Tanabe

2018

Cancer

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Molecular characterization of hepatocellular carcinoma (HCC) has greatly improved our understanding of disease pathogenesis. Mutational analysis, RNA and microRNA expression profiling, and epigenetic characterization have revealed common aberrations in oncogenes and tumor suppressors that correlate with disease biology and serve as a guide for the rational design of targeted therapies. These approaches have also led to the discovery of novel targets, including mutations in isocitrate dehydrogenase and chromatin remodeling enzymes. With the advent of immunotherapy, RNA expression profiling of the tumor microenvironment has identified a subset of HCC with high lymphocyte infiltration that may benefit from checkpoint inhibitor therapy. Molecular signatures thus capture the biology of a tumor, providing a supplement to current staging schema, which are based on tumor size and number, for more accurate prognostication of recurrence risk and survival. Molecular signatures may also be used to guide interventional therapy by defining those most suitable for transplantation or locoregional therapy rather than surgical resection. Finally, a multiomics approach involves the aggregation and analysis of multiple signatures for a more comprehensive characterization of pathogenic mechanisms. This broader approach attempts to address issues with signaling pathway cross-talk and redundancy, which have greatly limited the potential value of targeted therapies to date. Cancer 2018. © 2018 American Cancer Society.

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microRNA-23b suppresses epithelial-mesenchymal transition (EMT) and metastasis in hepatocellular carcinoma via targeting Pyk2

Cited by 37 publications

References 28 publications

Biological Effect and Mechanism of the miR-23b-3p/ANXA2 Axis in Pancreatic Ductal Adenocarcinoma

Biological Effect and Mechanism of the miR-23b-3p/ANXA2 Axis in Pancreatic Ductal Adenocarcinoma

miR‑23b suppresses lung carcinoma cell proliferation through CCNG1

Molecular signatures in hepatocellular carcinoma: A step toward rationally designed cancer therapy

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