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| 1 | Resveratrol induces AMPK and mTOR signaling inhibition-mediated autophagy and apoptosis in multiple myeloma cells显示文摘Resveratrol,a natural compound extracted from the skins of grapes,berries,or other fruits,has been shown to have anti-tumor effects against multiple myeloma(MM)via promoting apoptosis and inhibiting cell viability.In addition to apoptosis,autophagy also plays a significant role in anti-tumor effects.However,whether autophagy is involved in anti-MM activity of resveratrol remains unclear.In this study,human MM cell lines U266,RPMI-8226,and NCI-H929 were treated with resveratrol.Cell Counting Kit-8 assay and colony formation assay were used to measure cell viability.Western blot analysis was used to detect apoptosis-and autophagy-associated proteins.3-Methyladenine(3-MA)was applied to inhibit autophagy.Results showed that resveratrol inhibited cell viability and colony formation via promoting apoptosis and autophagy in MM cell lines U266,RPMI-8226,and NCI-H929.Resveratrol promoted apoptosis-related proteins,Caspase-3 activating poly-ADP-ribose polymerase and Caspase-3 cleavage,and decreased the protein level of Survivin in a dose-dependent manner.Additionally,resveratrol upregulated the levels of LC3 and Beclin1 in a dose-dependent way,indicating that autophagy might be implicated in anti-MM effect of resveratrol.Furthermore,3-MA relieved the cytotoxicity of resveratrol by blocking the autophagic flux.Resveratrol increased the phosphorylation of adenosine monophosphate(AMP)-activated protein kinase and decreased the phosphorylation of mammalian target of rapamycin(mTOR)and its downstream substrates p70S6K and 4EBP1 in a dose-dependent manner,leading to autophagy.Therefore,our results suggest that resveratrol exerts anti-MM effects through apoptosis and autophagy,which can be used as a new therapeutic strategy for MM in clinic. | Ruye Ma Dandan Yu Yu Peng Hongfei Yi Yingcong Wang Taofang Cheng Bingqing Shi Guang Yang Weiming Lai Xiaosong Wu Ye Lu Jumei Shi | 2021 | Acta Biochimica et Biophysica Sinica2021，53，6： | 7 |
| 2 | Quercetin inhibits the proliferation of multiple myeloma cells by upregulating PTPRR expression显示文摘Multiple myeloma (MM) is an incurable disease characterized by malignant plasma cell clonal expansion in the bone marrow;therefore, inhibiting the proliferation of plasma cells is an important approach to overcome the progression of MM. Quercetin (Que) is a promising flavonoid with broad-spectrum anti-tumor activity against various cancers, including MM;however, the underlying mechanism is not yet understood. The present study aimed to reveal the gene expression profile of Que-treated MM cells and clarify its potential mechanism. The 30% inhibitory concentration (IC30) of Que against MM cells was calculated, and the proliferation rate was significantly reduced after Que treatment. Next, 495 dysregulated genes were identified via RNA sequencing in Que-treated MM cells. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes analyses indicated that the dysregulated genes were enriched in various apoptosis-related GO terms and amino acid metabolism-related pathways. qPCR validation showed that protein tyrosine phosphatase receptor-type R (PTPRR) had the highest verified log2 FC (abs) among the top 15 dysregulated genes. Overexpression of PTPRR increased the sensitivity of MM cells against Que, significantly inhibiting their proliferation and colony formation ability;silencing of PTPRR showed the opposite results. Furthermore, bioinformatics analyses and PPI network construction of PTPRR indicated that dephosphorylation of ERK might be the potential pathway for the PTPRR-induced inhibition of MM cell proliferation. In summary, our study identified the gene expression profile in Que-treated MM cells and demonstrated that the upregulation of PTPRR was one of the important mechanisms for the Que-induced inhibition of MM cell proliferation. | Houcai Wang Dandan Yu Hui Zhang Ruye Ma Huiqun Wu Huili Zhai Huaping Wang Jingjing Li Liping Li Yingcong Wang Taofang Cheng Jumei Shi | 2021 | Acta Biochimica et Biophysica Sinica2021，53，11： | 2 |
| 3 | Anti-DLBCL efficacy of DCZ0825 in vitro and in vivo:involvement of the PI3K‒AKT‒mTOR/JNK pathway显示文摘Diffuse large B-cell lymphoma(DLBCL)is the most common type of non-Hodgkin lymphoma,characterized by high heterogeneity.The poor outcome of a portion of patients who suffer relapsing or resistant to conventional treatment impels the development of novel agents for DLBCL.DCZ0825 is a novel compound derived from pterostilbene and osalmide,whose antitumor activities have drawn our attention.In this study,we found that DCZ0825 exhibited high cytotoxicity toward DLBCL cell lines in a dose-and time-dependent manner,as revealed by cell counting kit-8 assay.Flow cytometry and western blot analysis results showed that DCZ0825 also promoted cell apoptosis via both extrinsic and intrinsic apoptosis pathways mediated by caspase.In addition,DCZ0825 induced cell cycle arrest in the G2/M phase by downregulating Cdc25C,CDK1,and Cyclin B1,thus interfering with cell proliferation.Further investigation showed the involvement of the phosphatidylinositol 3-kinase(PI3K)‒AKT‒mTOR/JNK pathway in the efficacy of DCZ0825 against DLBCL.Remarkably,DCZ0825 also exerted notable cytotoxic effects in vivo as well,with low toxicity to important internal organs such as the liver and kidney.Our results suggest that DCZ0825 may have the potential to become a novel anti-DLBCL agent or to replenish the conventional therapeutic scheme of DLBCL. | Ke Hu Bo Li Ruye Ma Hongfei Yi Zhijian Xu Yu Peng Dandan Yu Huiqun Wu Taofang Cheng Yumeng Lu Yong Zhang Rong Wei Guang Yang Xiaosong Wu Weiliang Zhu Jumei Shi | 2021 | Acta Biochimica et Biophysica Sinica2021，53，5： | 1 |
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