Abstract
The expression of miR-101 in carcinoma and para-carcinoma tissues of patients with liver cancer was studied. The carcinoma and para-carcinoma tissues of 67 patients with liver cancer treated in Chinese PLA General Hospital were collected, and the expression of miR-101 in carcinoma and para-carcinoma tissues was detected via reverse transcription-polymerase chain reaction (RT-PCR). The liver cancer HepG2 cell line was transfected with miR-101 mimics. Moreover, the influence of miR-101 overexpression on the proliferation of liver cancer cells was detected via Cell Counting Kit-8 assay and colony formation assay. The proportion of Ki67-positive cells in the control group (NC group) and miR-101 overexpression group (miR-101 mimics group) was detected via Ki67 staining. The proportions of cells were detected via flow cytometry, and the predicted target gene Zeste2 enhancer (EZH2) was further verified via luciferase reporter gene assay and western blotting. The miR-101 overexpression significantly inhibited the colony formation and proliferation ability of liver cancer cells (P<0.05). The proportion of Ki67-positive cells in liver cancer cells was lower in miR-101 mimics group (P<0.05). The proportion of cells in G0/G1 phase was increased in miR-101 mimics group compared with that in NC group (P<0.05). The extracellular signal-regulated kinase (ERK)1/2 phosphorylation level in liver cancer cells was obviously suppressed in miR-101 mimics group (P<0.05). Therefore, the expression level of miR-101 declines in liver cancer tissues, and the miR-101 overexpression can inhibit the proliferation of liver cancer cells. The inhibitory effect of miR-101 on the proliferation of liver cancer cells may be related to its inhibition on the mitogen-activated protein kinase (MAPK)/ERK signaling pathway, and the inhibition on the MAPK/ERK may be mediated by the targeted inhibition of miR-101 on EZH2.
Highlights
Primary liver cancer is one of the six most common cancers, and the number of deaths ranks 2nd in the total cancer‐related deaths [1]
The expression of miR‐101 in carcinoma and para‐carcinoma tissues was detected via RT‐PCR, and the results revealed that the expression level of miR‐101 in liver cancer tissues was significantly lower than that in para‐carcinoma tissues (P
At 0, 24, 48, 72 and 96 h after miR‐101 mimics were transfected into liver cancer cells, the cell proliferation in each group was detected using the Cell Counting Kit‐8 (CCK‐8) kit, and the optical density (OD) at 540 nm was used to reflect the proliferation ability
Summary
Primary liver cancer is one of the six most common cancers, and the number of deaths ranks 2nd in the total cancer‐related deaths [1]. The occurrence and development of liver cancer is a progressive cumulative complex process covering multiple factors, stages, mechanisms, links and genetic changes, which involves a variety of abnormal cellular or molecular changes, such as oxidative stress, endoplasmic reticulum stress and cell cycle disorder [3,4]. Clarifying the molecular mechanism for the occurrence and development of liver cancer has great significance in its early diagnosis and treatment. The PcG protein belongs to the polycomb repressive complex (PRC) family. PRC2 includes the Zeste enhancer (EZH2), suppressor of Zeste (SUZ12) and embryonic ectoderm development (EED) [6]. Increasingly more studies have revealed that EZH2 has a cancer‐promoting effect, including the induction of the abnormal cell differentiation and promotion of cancer cell proliferation [8]. It is reported in studies that the low expression of miR‐101 in glioma cells can lead to the upregulation of EZH2, thereby enhancing the proliferation, invasion and migration of glioma cells [10]
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