Abstract
Hepatocellular carcinoma (HCC) is one of the most common malignancy tumors with insidious onset, rapid development and metastasis, and poor prognosis. Therefore, it is necessary to understand molecular mechanisms of HCC and identify clinically useful biomarkers for it. This study aimed to investigate the role of retinoblastoma binding protein 5 (RBBP5) in HCC. The expression level of RBBP5 was examined by immunohistochemistry and western blot. The effect of RBBP5 on cell cycle, proliferation, apoptosis, and drug sensitivity was analyzed. RBBP5 was significantly upregulated in HCC tissues and cells. High RBBP5 expression was significantly associated with elevated level of AFP, advanced TNM stage, high Ki-67 expression, larger tumor size, and poor prognosis. Knockdown of RBBP5 significantly inhibited proliferation of HCC cells through cell cycle arrest. In addition, inhibition of RBBP5 increased the sensitivity of HCC cells to doxorubicin. In conclusion, our findings suggest that RBBP5 plays an important role in the progression of HCC and may serve as a novel biomarker and potential therapeutic target for HCC.
Highlights
Hepatocellular carcinoma (HCC) is the sixth most common cancer and the third most common cause of cancer-related death worldwide with insidious onset, rapid development and metastasis, and poor prognosis [1, 2]
Retinoblastoma binding protein 5 (RBBP5) is a core member of MLL/SET complexes involved in tumor cell cycle progression through an MLL–E2F axis which controls the expression of cyclins E, A, and B [11,12,13]
We investigated the effect of knockdown of RBBP5 on the proliferation, cell cycle, apoptosis, colon formation, and drug sensitivity of HCC cells
Summary
Hepatocellular carcinoma (HCC) is the sixth most common cancer and the third most common cause of cancer-related death worldwide with insidious onset, rapid development and metastasis, and poor prognosis [1, 2]. RBBP5 binds to underphosphorylated pRB1 in the regulation of cell cycle by RB1 pathway [6,7,8]. RBBP5 has been reported to be involved in a variety of tumors [9]. RBBP5 regulates DNA-damaging agent-induced apoptosis in tumor cells. RBBP5 is a core member of MLL/SET (mixed lineage leukemia/set-domain containing) complexes involved in tumor cell cycle progression through an MLL–E2F axis which controls the expression of cyclins E, A, and B [11,12,13]. RBBP5 is required for H3K4 methylation, which is a common marker of transcriptional activity in tumors, such as leukemia [11, 14]. The expression and precise role of RBBP5 in HCC remains virtually unknown
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