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Lentivirus-mediated TPD52L2 depletion inhibits the proliferation of liver cancer cells in vitro.

ABSTRACT: Tumor protein D52-like 2, known as hD54 in previous studies (TPD52L2), is a member of TPD52 family which has been implicated in multiple human cancers. In recent reports, TPD52 proteins were indicated to be associated with several malignancies, but very little is known about the function of TPD52L2 in liver cancers. In our present study, in order to explore the role of TPD52L2 in liver cancer, TPD52L2 was knocked down in SMMC-7721 liver cancer cell line by lentivirus mediated RNA interference. The results demonstrated that depletion of TPD52L2 could remarkably inhibit proliferation and colony forming ability of cancer cell SMMC-7721. Furthermore, cell cycle in TPD52L2 depleted cells was verified to be arrested in G0/G1 phase as determined by FACS assay, in consistence with the observation of cell proliferation inhibition. These results unraveled that TPD52L2 played an important role in tumorigenesis pathways of liver cancer and might serve as a promising target in human liver cancer diagnosis and therapy.

SUBMITTER: Pan ZY

PROVIDER: S-EPMC4402817 | biostudies-literature | 2015

REPOSITORIES: biostudies-literature

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Lentivirus-mediated TPD52L2 depletion inhibits the proliferation of liver cancer cells in vitro.

Pan Ze-Ya ZY Yang Yun Y Pan Hao H Zhang Jin J Liu Hui H Yang Yuan Y Huang Gang G Yin Lei L Huang Jian J Zhou Wei-Ping WP

International journal of clinical and experimental medicine 20150215 2

Tumor protein D52-like 2, known as hD54 in previous studies (TPD52L2), is a member of TPD52 family which has been implicated in multiple human cancers. In recent reports, TPD52 proteins were indicated to be associated with several malignancies, but very little is known about the function of TPD52L2 in liver cancers. In our present study, in order to explore the role of TPD52L2 in liver cancer, TPD52L2 was knocked down in SMMC-7721 liver cancer cell line by lentivirus mediated RNA interference. T ...[more]

PMID: 25932170

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Project description:Keratin 17 (KRT17) has been demonstrated to be a potential biological marker for the prediction of prognosis in particular types of cancer. The aim of the present study was to investigate the molecular mechanisms underlying the function of KRT17 in the pancreatic cancer (PAC) cell line PANC-1 and the potential of KRT17 as a therapeutic target for PAC. KRT17 expression levels were analyzed using quantitative PCR and compared with histological data using bioinformatics tools in PAC samples and three human PAC cell lines. Cell proliferation was determined using an MTT assay, in addition to cell cycle distribution and apoptosis analysis using flow cytometry, colony formation assay using Giemsa staining and cell motility analysis using a Transwell migration assay. Tumor growth was evaluated in vivo in nude mice. The expression levels of a number of signaling molecules were measured to establish the potential mechanism by which silencing KRT17 expression affected PAC PANC-1 cells. Increased levels of KRT17 expression were observed in human PAC compared with normal tissues, as well as in three human PAC cell lines (MIA PaCa-2, PANC-1 and KP-3 cells) compared with the H6c7 human immortal pancreatic duct epithelial cell line. High expression levels of KRT17 in PAC samples were associated with poor overall survival (P=0.036) and disease-free survival (P=0.017). Lentivirus-mediated KRT17 silencing inhibited cell proliferation, colony formation and migration, but promoted apoptosis and resulted in cell cycle arrest in the G0/G1 phase in PANC-1 cells. In addition, KRT17 knockdown inhibited in vivo tumor growth. KRT17 knockdown induced dysregulation of ERK1/2 and upregulation of the pro-apoptotic Bcl-2 protein Bad. In conclusion, the present study demonstrated that elevated KRT17 levels are positively associated with pancreatic cancer progression; KRT17 knockdown suppressed cell growth, colony formation, migration and tumor growth, and induced apoptosis and cell cycle arrest, affecting ERK1/2/Bad signaling. Therefore, the results of the present study suggested that KRT17 may be a potential target for the treatment of pancreatic cancer.

Project description:Purpose: Recent studies indicate that pregnancy upregulated non-ubiquitous calmodulin kinase (PNCK) is significantly up-regulated in breast and renal carcinomas. However, the expression profile and its biological relevance of PNCK in nasopharyngeal carcinoma (NPC) have not been elucidated. Methods: The expression level of PNCK was detected in specimens of NPC (n=10) and normal tissues (n=10) by real-time PCR and immunohistochemistry. Celigo Cell Counting and MTT assay were used to measure cell viability. Apoptosis was detected by flow cytometric analysis and caspases 3/7 activity assay. Real-time PCR and Western blotting were performed to evaluate the expression of PNCK. The bioluminescence imaging was used to evaluate the effects of PNCK knockdown on tumor growth using a xenograft animal model. The global gene expression profile was determined in wild type and PNCK-depleted CNE-2 cells via transcriptomics analysis. For mechanical investigation, the changes of PI3K/AKT/mTOR signaling pathway were detected by Western blotting. Results: The mRNA and protein levels of PNCK were increased in human NPC samples. In vitro experiments showed that shRNA or CRISPR-Cas9 mediated silencing of PNCK inhibited proliferation and induced apoptosis in NPC cells. In addition, in vivo assay revealed that knockdown of PNCK suppressed tumor growth. Consistently, a significant reduction of tumor bioluminescence in mice inoculated with PNCK-knockdown cells compared to that of control cells. In gene expression, the transcriptomics analysis revealed that there were 589 upregulated genes and 589 downregulated genes in PNCK-knockdown cells. Ingenuity Pathway Analysis (IPA) identified significant changes of PI3K/AKT/mTOR signaling pathway in PNCK-knockdown cells. Furthermore, western blot analysis revealed that interference with PNCK reduced the phosphorylation levels of PI3K, AKT and mTOR in CNE-2 cells. Conclusion: This study for the first time demonstrates that knockdown of PNCK could suppress growth and induce apoptosis of NPC cells both in vitro and in vivo by regulating PI3K/AKT/mTOR signaling pathway. These findings suggest that PNCK might be a novel therapeutic target for NPC treatment.

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Lentivirus-mediated TPD52L2 depletion inhibits the proliferation of liver cancer cells in vitro.

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Lentivirus-mediated TPD52L2 depletion inhibits the proliferation of liver cancer cells in vitro.

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