MiR‐106b regulates the apoptosis and tumorigenesis of hepatocellular carcinoma via targeting Zinc finger and BTB domain‐containing protein 7A (Zbtb7a)

Abstract

MicroRNAs play vital regulatory roles in various type of tumorigenesis. We aimed to explore the functional microRNAs that might play as therapeutic targets in hepatocellular carcinoma (HCC). In this study, our results revealed that microRNA-106b was significantly increased in HCC tumor tissues. However, miR-106b knockdown remarkably suppressed the growth and increased the apoptosis of Hub-7 HCC cells. Biological analysis indicated that miR-106b directly targeted toZinc finger and BTB domain-containing protein 7A (Zbtb7a) to regulate the apoptosis of Hub-7 cells. Extensively, Zbtb7a overexpression reversed Huh-7 cell apoptosis and growth in vitro. Furthermore, in vivo studies confirmed that miR-106b inhibition or Zbtb7a overexpression retarded the growth of Hub-7 xenograft tumor in nude mice. In conclusion, we provide the evidence for the regulatory role of miR-106b in HCC, which is causally linked to targeting of Zbtb7a. This study may provide miR-106b as a potential therapeutic strategy for HCC.

The miR-372-ZBTB7A Oncogenic Axis Suppresses TRAIL-R2 Associated Drug Sensitivity in Oral Carcinoma

“…In previous studies, miR-20a, miR-100 and miR-125a have been shown to be suppressor miRNAs that are able to reduce expression of the ZBTB7A proto-oncogene in tumors (26)(27)(28). However, it has been found that miR-106b targeting of ZBTB7A increases the survival of hepatocellular carcinoma cells (25). This study further identifies that ZBTB7A is also under the post-transcriptional control of miR-372 in addition to there being gene copy loss during oral tumorigenesis.…”

“…However, studies also found that ZBTB7A may also interact with and repress SOX9 (sex determining region Y-box 9), various glycolytic transcription factors and a number of other targets; these findings reveal this protein's functional complexity when mediating tumor suppression (16,17,(19)(20)(21)(22). Although the roles of ZBTB7A in carcinogenesis are controversial and the mechanisms by which it acts remain largely obscure, frequent deletion and downregulation of ZBTB7A has been shown to occur in a range of malignancies including OSCC (20,(23)(24)(25). In addition, miR-106b and other miRNAs have been shown to target ZBTB7A in such malignancies (25)(26)(27)(28).…”

“…Although the roles of ZBTB7A in carcinogenesis are controversial and the mechanisms by which it acts remain largely obscure, frequent deletion and downregulation of ZBTB7A has been shown to occur in a range of malignancies including OSCC (20,(23)(24)(25). In addition, miR-106b and other miRNAs have been shown to target ZBTB7A in such malignancies (25)(26)(27)(28).…”

Incorporating MicroRNA into Molecular Phenotypes of Circulating Tumor Cells Enhances the Prognostic Accuracy for Patients with Metastatic Breast Cancer

“…It has been reported that overexpression of miR‐106b was observed in a variety of human tumors, which plays an oncogenic role in tumor progression and prognosis, including colorectal cancer , gastric cancer , hepatocellular carcinoma , glioma tumors , renal cell carcinoma , and head and neck squamous cell carcinomas . MiR‐106b plays a functional role in promoting proliferation, migration, and invasion of cancer cells both in vitro and in vivo . Clinical data show that high expression level of miR‐106b is associated with metastasis and poor prognosis .…”

Retracted Article: Exosome-derived PTENP1 suppresses cisplatin resistance of bladder cancer (BC) by suppressing cell proliferation, migration and inducing apoptosis via the miR-103a/PDCD4 axis

“…MicroRNAs (miRNA) are small non-protein coding RNAs that regulate gene expression at post-transcriptional level. 14 They participate in the pathological process of many diseases by regulating cell metabolism, inammation, migration, autophagy, apoptosis and drug resistance. [15][16][17] For example, reduced expression of miR-103a improved epilepsy induced neuron injury in rats by activating astrocytes in hippocampus through interacting with BDNF.…”