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Ribosomal protein L34 promotes the proliferation, invasion and metastasis of pancreatic cancer cells.

ABSTRACT: Ribosomal proteins (RPs) are the main components of ribosomes and participate in the self-assembly of ribosomes and protein synthesis. Recent advance has shown that RPs play important roles in the tumorigenesis and drug resistance of various cancers. However, the expression status and function of RPL34 in pancreatic cancer (PC) remains unclear. In this study, we find that RPL34 is overexpressed in PC tissues and cell lines, which is correlated with decreased methylation of its promoter. Knockdown of RPL34 effectively suppresses the proliferation, colony formation, migration and drug-resistance of PC cells, which are accompanied by cell cycle arrest at the G2 phase and induction of apoptosis. In vivo assays demonstrate that RPL34 silencing inhibits PC tumor growth and metastasis. Moreover, gene expression profiling revealed that RPL34 silencing results in alteration of the MAPK and p53 signaling pathways. Clinically, our data indicate a positive association of RPL34 expression with tumor stage and metastasis in PCs. We revealed that RPL34 acts as a potential onco-protein in PC, and RPL34 may be a promising biomarker for prognosis prediction and a potential target for the treatment of PC.

SUBMITTER: Wei F

PROVIDER: S-EPMC5356734 | biostudies-literature | 2016 Dec

REPOSITORIES: biostudies-literature

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Ribosomal protein L34 promotes the proliferation, invasion and metastasis of pancreatic cancer cells.

Wei Feng F Ding Lijuan L Wei Zhentong Z Zhang Yandong Y Li Yang Y Qinghua Luo L Ma Yuteng Y Guo Liang L Lv Guoyue G Liu Yan Y

Oncotarget 20161201 51

Ribosomal proteins (RPs) are the main components of ribosomes and participate in the self-assembly of ribosomes and protein synthesis. Recent advance has shown that RPs play important roles in the tumorigenesis and drug resistance of various cancers. However, the expression status and function of RPL34 in pancreatic cancer (PC) remains unclear. In this study, we find that RPL34 is overexpressed in PC tissues and cell lines, which is correlated with decreased methylation of its promoter. Knockdow ...[more]

PMID: 27845896

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Project description:Background: Exogenous HMGB1 plays a vital role in tumor recurrence, and HMGB1 is ubiquitous in the tumor microenvironment. However, the mechanism of action is still unclear. We investigated the role of exogenous HMGB1 in tumor proliferation and metastasis using human SW1990 and PANC-1 cells after radiotherapy and explored the possible molecular mechanism. Materials and Methods: Residual PANC-1 cells and SW1990 cells were isolated after radiotherapy. The supernatant after radiotherapy was collected. The relative expression of HMGB1 was evaluated by Enzyme Linked Immunosorbent Assay (ELISA). Electron microscope (EMS) was used to collect the images of pancreatic cancer cells pre and post radiotherapy treatment. The proliferation of pancreatic cancer cells which were treated with different radiation doses was measured by Carboxy Fluorescein Succinimidyl Ester (CFSE). The migration rates of pancreatic cancer cells were measured by wound healing assays. Subsequently, the expression of related proteins was detected by Western Blot. In vivo, the subcutaneous pancreatic tumor models of nude mice were established, and therapeutic capabilities were tested. Results: HMGB1 was detected in the supernatant of pancreatic cancer cells after radiotherapy. The results of CFSE showed that exogenous HMGB1 promotes the proliferation and metastasis of pancreatic cancer cells. The western blot results showed activation of p-GSK 3β and up-regulation of N-CA, Bcl-2, and Ki67 in response to HMGB1 stimulation, while E-CA expression was down-regulated in pancreatic cancer cells in response to HMGB1 stimulation. In vivo, ethyl pyruvate (EP, HMGB1 inhibitor) inhibits the growth of tumors and HMGB1 promotes the proliferation of tumors after radiation. Conclusion: Radiotherapy induces HMGB1 release into the extracellular space. Exogenous HMGB1 promotes the proliferation and metastasis of PANC-1 cells and SW1990 cells by activation of p-GSK 3β which is mediated by Wnt pathway.

Dataset Information

Ribosomal protein L34 promotes the proliferation, invasion and metastasis of pancreatic cancer cells.

Publications

Ribosomal protein L34 promotes the proliferation, invasion and metastasis of pancreatic cancer cells.

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