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-  2019 

LATS2 overexpression attenuates the therapeutic resistance of liver cancer HepG2 cells to sorafenib-mediated death via inhibiting the AMPK–Mfn2 signaling pathway

DOI: 10.1186/s12935-019-0778-1

Keywords: HCC, Mitophagy, Sorafenib, AMPK pathway, LATS2

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Abstract:

LATS2 overexpression increases sorafenib-mediated cell death in HepG2 liver cancer cells in vitro. a, b Different doses of sorafenib was added into the medium of HepG2 cells and then the expression of LATS2 was determined via western blotting. c RNA was isolated from HepG2 cells after exposure to sorafenib and then the transcription of LATS2 was evaluated via qPCR. d Cellular viability was measured via MTT assay. Different doses of sorafenib was added into the medium of HepG2 cells. e, f Adenovirus transfection was used to perform the overexpression assay of LATS2 in the presence of sorafenib treatment. The overexpression efficiency was confirmed via western blotting. g LDH release assay was used to evaluate cell death in response to sorafenib treatment and/or LATS2 overexpression. h Caspase-3 activity of HepG2 cells. Adenovirus-loaded LATS2 (Ad-LATS2) was transfected into HepG2 cells in the presence of sorafenib. i, j TUNEL assay for apoptotic cells. The number of apoptotic cells was recorded. Adenovirus-loaded LATS2 was transfected into HepG2 cells in the presence of sorafenib. *p?<?0.05 vs. control group; #p?<?0.05 vs. Sorafenib?+?Ad-cont grou

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