期刊
CELL DEATH & DISEASE
卷 10, 期 -, 页码 -出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/s41419-019-1320-z
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资金
- Clinical Medical Research Center of Hepatobiliary Surgery of Guizhou Province, Platform Talent of Scientific Collaboration of Guizhou Province [[2017] 5404]
- High-Level Innovative Talent Training Program Ten Level Talents of Guizhou Province, Platform Talent of Scientific Collaboration of Guizhou Province [[2016] 5647]
- Brainstorm Project on Social Development by the Department of Science and Technology of Guizhou Province [SY [2015] 3047]
- Youth Science and Technology Talent Growth Project by the Department of Education of Guizhou Province [[2016] 142]
- Tutor Studio of Sun Chengyi's Diagnosis and Treatment of Hepatobiliary, Pancreatic and Splenic Diseases, Teaching and Research Collaboration of Guizhou Province [GZS [2016] 09]
- Department of Science and Technology of Guizhou Province, Hepatobiliary Surgery, Station of Academician Workstation of Guiyang Medical College, Academician Station of Scientific Collaboration of Guizhou Province [[2015] 4013]
- United Fund of the Department of Science and Technology of Guizhou Province and Affiliated Hospital of Guizhou Medical University, Scientific Collaboration of Guizhou Province [LH [2016] 7229]
- Fund of The Fourth Talent Base of Guizhou Province
- Special Collaboration of Guizhou Province [[2012]94]
The poor prognosis of patients with pancreatic ductal adenocarcinoma (PDAC) is partially attributed to the invasive and metastatic behavior of this disease. Laminin subunit beta-3 (LAMB3) encodes one of the three subunits of LM-332, an extracellular matrix protein secreted by cultured human keratinocytes. In addition, LAMB3 is involved in the invasive and metastatic abilities of some types of cancer, including colon, pancreas, lung, cervix, stomach, and prostate cancer, but the role and mechanism of LAMB3 in PDAC have not been previously determined. Herein, we tentatively investigated the role of LAMB3 in the malignant biological behavior of PDAC. In this study, we demonstrated that LAMB3 is upregulated in PDAC. Inhibition of LAMB3 abrogated the tumorigenic outcomes of PI3K/Akt signaling pathway activation, including those involving cell cycle arrest, cell apoptosis, proliferation, invasion and migration in vitro, and tumor growth and liver metastasis in vivo. Our results showed that LAMB3 could mediate cell cycle arrest and apoptosis in PDAC cells and alter the proliferative, invasive, and metastatic behaviors of PDAC by regulating the PI3K/Akt signaling pathway. LAMB3 may be a novel therapeutic target for the treatment of PDAC in the future.
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