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JQ1, a BET‐bromodomain inhibitor, inhibits human cancer growth and suppresses PD‐L1 expression
Author(s) -
Liu Kaisheng,
Zhou Zhifan,
Gao Hengyuan,
Yang Fang,
Qian Yajun,
Jin Hongtao,
Guo Yaomin,
Liu Ying,
Li Haili,
Zhang Cheng,
Guo Jinan,
Wan Yong,
Chen Rui
Publication year - 2019
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1002/cbin.11139
Subject(s) - bromodomain , cancer research , cancer , growth inhibition , cancer cell , cell growth , cytotoxic t cell , cell culture , apoptosis , messenger rna , biology , lung cancer , cell , chemistry , medicine , in vitro , biochemistry , epigenetics , genetics , gene
Most traditional cytotoxic chemotherapeutic agents have poor aqueous solubility and significant toxicity. Hence, there is a need to develop molecule‐targeted drugs. Programmed death‐ligand 1 (PD‐L1) is associated with the prognosis of several cancer types, and blockade of PD‐1/PD‐L1 signaling increases the amplitude of anti‐tumor immunity. In the present study, we investigated the effects of JQ1, a bromodomain and extraterminal‐bromodomain inhibitor, on cell growth, and messenger RNA (mRNA) and protein levels of PD‐L1 in renal cell carcinoma primary culture cells, and prostate, liver, and lung cancer cell lines. The results of the cell counting kit‐8 assay suggested that JQ1 inhibits cell growth in a dose‐dependent manner. The mRNA and protein levels of PD‐L1 decreased in the primary culture of JQ1‐treated renal carcinoma, prostate cancer, liver cancer, and lung cancer cell lines. In addition, the mRNA level of PD‐L2 also decreased in the JQ1‐treated cells. Overall, JQ1 might be a potential anti‐tumor agent.