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Retracted : Smad4 gene silencing enhances the chemosensitivity of human lymphoma cells to adriamycin via inhibition of the activation of transforming growth factor β signaling pathway
Author(s) -
Li Qiuhuan,
Liu Xiaoyu,
Zhao Chuanli
Publication year - 2019
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.28772
Subject(s) - gene silencing , small hairpin rna , raji cell , apoptosis , cancer research , signal transduction , cell growth , rna interference , microbiology and biotechnology , biology , transforming growth factor , messenger rna , cell , gene , rna , gene knockdown , biochemistry
Abstract There are diverse investigations focused on the therapies of lymphoma. Our research was taken to identify the effects of lentiviral‐mediated Smad4 gene silencing on chemosensitivity of human lymphoma cells to adriamycin (ADM) via transforming growth factor β (TGFβ) signaling pathway. Raji/ADM cells were cultured and infected with lentiviral particles Smad4‐short hairpin (shRNA) and control‐shRNA. Then, the messenger RNA (mRNA) and protein levels of TGFβ signaling pathway–related factors (Smad4, Smad3, cyclinE, cyclinD1, and p21) in Raji/ADM cells were determined. The effect of Smad4‐shRNA on cell viability, invasion and migration, and apoptosis were also detected. Compared with the Raji group, increased mRNA and protein levels of Smad4, Smad3, cyclinE, cyclinD1, enhanced cell proliferation, migration and invasion as well as decreased mRNA, and protein levels of p21 and cell apoptosis rate were found in the Raji/ADM and control‐shRNA groups. However, Smad4 gene silencing resulted in decreased mRNA and protein levels of Smad4, Smad3, cyclinE, and cyclinD1 along with inhibited cell proliferation, migration and invasion but increased expression of p21 together with cell apoptosis. Collectively, Smad4 gene silencing can inhibit the activation of TGFβ signaling pathway, thereby enhancing the chemosensitivity of human lymphoma cells to ADM.