Please use this identifier to cite or link to this item: https://doi.org/10.1016/j.jare.2021.02.002
Title: PIK3CB is involved in metastasis through the regulation of cell adhesion to collagen I in pancreatic cancer
Authors: Qu, Jianhua 
Zheng, Biao
Ohuchida, Kenoki
Feng, Haimin
Chong, Stephen Jun Fei
Zhang, Xianbin
Liang, Rui
Liu, Zhong
Shirahane, Kengo
Mizumoto, Kazuhiro
Gong, Peng
Nakamura, Masafumi
Keywords: Adhesion
Collagen I
Metastasis
Pancreatic cancer
PIK3CB
Issue Date: 1-Feb-2021
Publisher: Elsevier B.V.
Citation: Qu, Jianhua, Zheng, Biao, Ohuchida, Kenoki, Feng, Haimin, Chong, Stephen Jun Fei, Zhang, Xianbin, Liang, Rui, Liu, Zhong, Shirahane, Kengo, Mizumoto, Kazuhiro, Gong, Peng, Nakamura, Masafumi (2021-02-01). PIK3CB is involved in metastasis through the regulation of cell adhesion to collagen I in pancreatic cancer. Journal of Advanced Research 33 : 127-140. ScholarBank@NUS Repository. https://doi.org/10.1016/j.jare.2021.02.002
Rights: Attribution-NonCommercial-NoDerivatives 4.0 International
Abstract: Introduction: Pancreatic adenocarcinoma (PAAD) is an aggressive malignancy, with a major mortality resulting from the rapid progression of metastasis. Unfortunately, no effective treatment strategy has been developed for PAAD metastasis to date. Thus, unraveling the mechanisms involved in PAAD metastatic phenotype may facilitate the treatment for PAAD patients. Objectives: PIK3CB is an oncogene implicated in cancer development and progression but less is known about whether PIK3CB participates in PAAD metastasis. Therefore, the objective of this study is to explore the mechanism(s) of PIK3CB in PAAD metastasis. Methods: In our study, we examined the PIK3CB expression pattern using bioinformatic analysis and clinical material derived from patients with PAAD. Subsequently, a series of biochemical experiments were conducted to investigate the role of PIK3CB as potential mechanism(s) underlying PAAD metastasis in vivo using nude mice and in vitro using cell lines. Results: We observed that PIK3CB was involved in PAAD progression. Notably, we identified that PIK3CB was involved in PAAD metastasis. Downregulation of PIK3CB significantly reduced PAAD metastatic potential in vivo. Furthermore, a series of bioinformatic analyses showed that PIK3CB was involved in cell adhesion in PAAD. Notably, PIK3CB depletion inhibited invasion potential specifically via suppressing cell adhesion to collagen I in PAAD cells. Conclusion: Collectively, our findings indicate that PIK3CB is involved in PAAD metastasis through cell-matrix adhesion. We proposed that PIK3CB is a potential therapeutic target for PAAD therapy. © 2021
Source Title: Journal of Advanced Research
URI: https://scholarbank.nus.edu.sg/handle/10635/233628
ISSN: 2090-1232
DOI: 10.1016/j.jare.2021.02.002
Rights: Attribution-NonCommercial-NoDerivatives 4.0 International
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