miR-217 suppresses proliferation, migration, and invasion promoting apoptosis via targeting MTDH in hepatocellular carcinoma

Zhang, Mao; Li, Min; Li, Na; Zhang, Zilang; Liu, Ning; Han, Xiaoyu; Liu, Qincheng; Liao, Cai-xian

doi:10.3892/or.2017.5401

Cited by 40 publications

(30 citation statements)

References 31 publications

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“…The MTDH increases cell survival by promoting survival pathways such as PI3K and NF‐κB. Regulation of cell proliferation and metastasis via MTDH‐mediated autophagy is mediated by several miRNA, such as miR‐1297, miR‐145, miR‐98, and miR‐217. Our studies further revealed that miR‐22 increased the chemosensitivity through the miR‐22/MTDH/autophagy regulatory loop.…”

Section: Discussionsupporting

confidence: 55%

Roles of microRNA‐22 in Suppressing Proliferation and Promoting Sensitivity of Osteosarcoma Cells via Metadherin‐mediated Autophagy

Wang

Zhao

Guo

et al. 2019

Orthopaedic Surgery

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Objective To analyze the effect of microRNA‐22 on autophagy and proliferation and to investigate the underlying molecular mechanism of osteosarcoma cell chemotherapy sensitivity. Methods MG‐63 cells were divided into four groups, including a control group, a negative control (NC) group, a cisplatin group, and a cisplatin + miR‐22 group. Proliferation of MG‐63 cells that had been treated with cisplatin and transfected with miR‐22 mimics was determined using MTT assay and colony formation assay. We assessed the degree of autophagy using flow cytometry through cellular staining of the autophagy lysosomal marker monodansylcadaverine (MDC). The effect of microRNA‐22 on autophagy was observed along with the expression levels of Beclin1, LC3, metadherin (MTDH) and ATG5 by western blot and quantitative reverse transcription polymerase chain reaction (qRT‐PCR). Luciferase reporter assay revealed the targeted binding site between miR‐22 and the 3′‐untranslated region (3′‐UTR) of MTDH mRNA. Western blot and qRT‐PCR were used to explore the level of MTDH in the control group, the NC group, the cisplatin group, and the miR‐22 group for 6, 12, and 24 h. Results In the in vitro study, the MTT results indicated that the MG‐63 cells with overexpression of miR‐22 exhibited a significant decline in the proliferation capacity compared with the control group (0.513 ± 0.001, P < 0.0005). Similar to the MTT results, MG‐63 cells that were transfected with miR‐22 mimic (101.0 ± 10.58) formed fewer colonies compared with the cisplatin group (129.7 ± 4.163). MDC staining revealed that miR‐22‐overexpressing osteosarcoma (OS) cells treated with cisplatin showed a significant decrease in the expression of autophagy (7.747 ± 0.117, P < 0.0001). Our data revealed that miR‐22 could regulate not only autophagy but also proliferation in the chemosensitivity of osteosarcoma cells. We found that miR‐22 sensitized osteosarcoma cells to cisplatin treatment by regulating autophagy‐related genes. In addition, Luciferase Reporter Assay revealed that miR‐22 negatively regulated autophagy through direct targeting of MTDH. We performed western blot analysis to detect the MTDH expression level. The results revealed that the overexpression of miR‐22 obviously decreased the expression of MTDH (1.081 ± 0.023, P < 0.001). Conclusion Inhibition of miR‐22 ameliorated the anticancer drug‐induced cell proliferation decrease in osteosarcoma cells. MTDH was identified as the miR‐22 target in OS cells and MTDH‐triggered autophagy played a key function in the miR‐22‐associated chemotherapy sensitivity.

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Section: Discussionsupporting

confidence: 55%

Roles of microRNA‐22 in Suppressing Proliferation and Promoting Sensitivity of Osteosarcoma Cells via Metadherin‐mediated Autophagy

Wang

Zhao

Guo

et al. 2019

Orthopaedic Surgery

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“…The EMT has an important role in tumor cell migration and invasion, and MTDH has been reported to be a contributor to EMT (27). In our study, we showed that MTDH is modulated by SNHG1; therefore, we speculated that SNHG1 also participates in the EMT process.…”

Section: The Snhg1 Regulatory Network Functioned In Nsclc Cellsmentioning

confidence: 48%

Long noncoding RNASNHG1promotes non‐small cell lung cancer progression by up‐regulatingMTDH viasponging miR‐145–5p

Shan

et al. 2018

FASEB j.

124

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Long noncoding RNAs participate in the progression and initiation of non-small cell lung cancer (NSCLC), although the mechanism remains unknown. The lncRNA identified as small nucleolar RNA host gene 1 ( SNHG1) is a novel lncRNA that is increased in multiple human cancers; however, the regulatory mechanism requires further investigation. In this study, we discovered that SNHG1 was markedly up-regulated in NSCLC tissues and cells and that SNHG1 silencing decreased tumor volumes. Moreover, we explored its regulatory mechanism and found that SNHG1 directly bound to microRNA (miRNA)-145-5p, isolating miR-145-5p from its target gene MTDH. Inhibition of SNHG1 suppressed NSCLC cell viability, proliferation, migration, and invasion in vitro, but its effect was rescued by miR-145-5p inhibition. These results demonstrate that SNHG1 contributes to NSCLC progression by modulating the miR-145-5p/ MTDH axis, and it could potentially be a therapeutic target as well as a diagnostic marker.-Lu, Q., Shan, S., Li, Y., Zhu, D., Jin, W., Ren, T. Long noncoding RNA SNHG1 promotes non-small cell lung cancer progression by up-regulating MTDH via sponging miR-145-5p.

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“…miRNAs are involved in regulation of the cell cycle and proliferation of HCC cells 49 , 50 . We previously reported that, for arsenite-transformed HaCat cells, circRNA_100284 regulates the cell cycle by acting as a sponge of miR-217 15 , a tumor suppressor that regulates cell proliferation in various cancers, including HCCs 51 . miR-217 inhibits cell proliferation through inducing arrest in the G2/M phase of the cell cycle 52 .…”

Section: Discussionmentioning

confidence: 99%

Exosomal circRNA_100284 from arsenite-transformed cells, via microRNA-217 regulation of EZH2, is involved in the malignant transformation of human hepatic cells by accelerating the cell cycle and promoting cell proliferation

et al. 2018

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Intercellular communication between malignant cells and neighboring nonmalignant cells is involved in carcinogenesis. In the progression of carcinogenesis, exosomes are messengers for intercellular communication. Circular RNAs (circRNAs) are noncoding RNAs with functions that include regulation of the cell cycle and proliferation. However, the functions of exosomal circRNAs are not clear. The present research aimed to determine whether circRNAs secreted from arsenite-transformed human hepatic epithelial (L-02) cells are transferred into normal L-02 cells and become functionally active in the normal cells. The results showed that circRNA_100284 is involved in the malignant transformation of L-02 cells induced by arsenite. The medium from transformed L-02 cells induced upregulation of circRNA_100284, accelerated the cell cycle, and promoted proliferation of normal L-02 cells. Transformed cells transferred circRNA_100284 into normal L-02 cells via exosomes and led to the malignant transformation of the non-transformed cells. Knockdown of circRNA_100284, which reduced circRNA_100284 levels in exosomes derived from transformed L-02 cells, blocked the accelerated cell cycle and reduced proliferation and malignancy. In addition, in normal L-02 cells, exosomal circRNA_100284 derived from arsenite-transformed L-02 cells induced acceleration of the cell cycle and promoted proliferation via acting as a sponge of microRNA-217. Further, exosomal circRNA_100284 was upregulated in the sera of people exposed to arsenite. Thus, exosomes derived from transformed L-02 cells transferred circRNA_100284 to surrounding cells, which induced an accelerated cell cycle and promoted proliferation of normal liver cells and led to the malignant transformation of the non-transformed cells. The findings support the concept that exosomal circRNAs are involved in cell–cell communication during carcinogenesis induced by arsenite.

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miR-217 suppresses proliferation, migration, and invasion promoting apoptosis via targeting MTDH in hepatocellular carcinoma

Cited by 40 publications

References 31 publications

Roles of microRNA‐22 in Suppressing Proliferation and Promoting Sensitivity of Osteosarcoma Cells via Metadherin‐mediated Autophagy

Roles of microRNA‐22 in Suppressing Proliferation and Promoting Sensitivity of Osteosarcoma Cells via Metadherin‐mediated Autophagy

Long noncoding RNASNHG1promotes non‐small cell lung cancer progression by up‐regulatingMTDH viasponging miR‐145–5p

Exosomal circRNA_100284 from arsenite-transformed cells, via microRNA-217 regulation of EZH2, is involved in the malignant transformation of human hepatic cells by accelerating the cell cycle and promoting cell proliferation

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