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

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.

Proteasomal cysteine deubiquitinase inhibitor b-AP15 suppresses migration and induces apoptosis in diffuse large B cell lymphoma

“…Upregulation of CXC chemokine ligand 9 promotes viability and migration that can be abolished by knocking down of β-catenin in DLBCL cells [28], suggesting that Wnt/β-catenin signaling pathway plays an important role in DLBCL cell migration. Moreover, in Raji/ADM cells (B-cell non-Hodgkin’s lymphomas), inhibiting the activation of TGFβ signaling pathway via silencing Smad4 contributes to the suppression of cell viability, invasion and migration [29]. In addition, previous studies have shown that USP14 is an important regulator in Wnt/β-catenin signaling pathway by deubiquitinating Dvl [30].…”

Inhibitory effect of dihydromyricetin on the proliferation of JAR cells and its mechanism of action

“…The SMAD2/3/4 complex is translocated to the nucleus, where it binds to DNA and regulates the transcription of several genes (31,32). Increased mRNA and protein expression levels of SMAD3 and SMAD4 promote cell proliferation, migration and invasion (33). Previous studies have shown that the TGF-β/SMAD signaling pathway can regulate the proliferation of choriocarcinoma cells (15,16).…”