Synergistic Effect and Molecular Mechanism of Homoharringtonine and Bortezomib on SKM-1 Cell Apoptosis

The transcription factor Sox2 [SRY (sex-determining region Y)-box 2] is essential for the regulation of self-renewal and homoeostasis of NSCs (neural stem cells) during brain development. However, the downstream targets of Sox2 and its underlying molecular mechanism are largely unknown. In the present study, we found that Sox2 directly up-regulates the expression of survivin, which inhibits the mitochondria-dependent apoptotic pathway in NSCs. Although overexpression of Sox2 elevates survivin expression, knockdown of Sox2 results in a decrease in survivin expression, thereby initiating the mitochondria-dependent apoptosis related to caspase 9 activation. Furthermore, cell apoptosis owing to knockdown of Sox2 can be rescued by ectopically expressing survivin in NSCs as well as in the mouse brain, as demonstrated by an in utero-injection approach. In short, we have found a novel Sox2/survivin pathway that regulates NSC survival and homoeostasis, thus revealing a new mechanism of brain development, neurological degeneration and such aging-related disorders.

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Raman Spectroscopy–Based Multivariate Statistical Analysis Reveals the Molecular Mechanism of K562 Cell Apoptosis Induced by Adriamycin

Spectroscopy Letters ◽

10.1080/00387010.2013.803207 ◽

2014 ◽

Vol 47 (4) ◽

pp. 301-305 ◽

Cited By ~ 5

Author(s):

Tao Tao ◽

Qi Shen ◽

Xiaoxu Lu ◽

Yingtian He ◽

Liyun Zhong

Keyword(s):

Raman Spectroscopy ◽

Statistical Analysis ◽

Molecular Mechanism ◽

Multivariate Statistical Analysis ◽

Cell Apoptosis ◽

K562 Cell ◽

Multivariate Statistical

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MicroRNA-497-5p Functions as a Modulator of Apoptosis by Regulating Metadherin in Ovarian Cancer

Cell Transplantation ◽

10.1177/0963689719897061 ◽

2020 ◽

Vol 29 ◽

pp. 096368971989706 ◽

Cited By ~ 1

Author(s):

Chunyan Liu ◽

Anne Bordeaux ◽

Stanka Hettich ◽

Suhui Han

Keyword(s):

Ovarian Cancer ◽

Mortality Rate ◽

Molecular Mechanism ◽

High Mortality ◽

Cell Apoptosis ◽

Untranslated Region ◽

Protein Levels ◽

Enhanced Expression ◽

Related Proteins

Ovarian cancer (OC) has a high mortality rate among women worldwide. However, even with the advances in detection and therapeutics, the number of cases is increasing worldwide. Increasingly, microRNAs (miRNAs), including miR-497-5p, have been implicated in the progression of many cancers, but the role of miR-497-5p in OC remains unknown. The purpose of this study was to investigate the underlying molecular mechanism of miR-497-5p in OC. Herein, we find that miR-497-5p is down-regulated in OC tissues, and overexpression of miR-497-5p enhances apoptosis in OC cells. The increased apoptosis was correlated with enhanced expression of apoptosis-related proteins. MiR-497-5p directly bound the 3’-untranslated region of metadherin (MTDH), leading to the reduction of MTDH in mRNA and protein levels. Moreover, MTDH knockout promoted the apoptosis of OC cells. Taken together, we conclude that miR-497-5p contributes to cell apoptosis in OC by regulating MTDH.

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M1569 The Molecular Mechanism of Norepinephrine Induced In Vitro Hepatic Stellate Cell Apoptosis

Gastroenterology ◽

10.1016/s0016-5085(08)63716-6 ◽

2008 ◽

Vol 134 (4) ◽

pp. A-795

Author(s):

Xiaolan Zhang ◽

Na Liu ◽

Dongmei Yao ◽

Xiaopeng Tian

Keyword(s):

Molecular Mechanism ◽

Hepatic Stellate Cell ◽

Cell Apoptosis ◽

Stellate Cell

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METTL3 promotes inflammation and cell apoptosis in a pediatric pneumonia model by regulating EZH2

Allergologia et Immunopathologia ◽

10.15586/aei.v49i5.445 ◽

2021 ◽

Vol 49 (5) ◽

pp. 49-56

Author(s):

Xiaoqing Yang ◽

Ying Yang ◽

Yi Wu ◽

Meijiao Fu

Keyword(s):

Inflammatory Response ◽

Protein Expression ◽

Western Blot ◽

Cell Viability ◽

Molecular Mechanism ◽

Cell Apoptosis ◽

Cell Model ◽

Medical Science ◽

Blood Monocytes ◽

Pediatric Pneumonia

Background: In recent times, the medical science has developed by leaps and bounds, however, the molecular mechanism of pediatric pneumonia is still unclear. Although prior researches have shown that methyltransferase-like 3 (METTL3) is up-regulated in a variety of inflammatory diseases, its role and mechanism has been rarely studied in pediatric pneumonia, and need to be defined elaborately.Objective: In this study, the related molecular mechanism of METTL3 on inflammation and cell apoptosis in a pediatric pneumonia was investigated. Materials and methods: Quantitative real-time polymerase chain reaction (qPCR) and western blot assays were employed to examine the mRNA and protein expression level of METTL3 and EZH2 in peripheral blood monocytes from pediatric pneumonia patients or cell model (WI-38). Then, qPCR and ELISA assay were applied to verify the inflammatory response in LPS-treated WI-38 cell lines after knockdown of METTL3. Besides, MTT cell viability assays, flow cytometry, and western blot assays were applied to examine the cell viability and cell apoptosis of LPS-treated WI-38 cell after knockdown of METTL3. Further, the western blot assays were employed to examine the protein expression levels of p-JAK2, JAK2, p-STAT3, STAT3, and EZH2 in LPS-treated WI-38 cell after knockdown of METTL3. Finally, ELISA and western blot were applied to verify the inflammatory response and cell apoptosis of LPS-treated WI-38 cell after knockdown of METTL3 and overexpression of EZH2.Results: In this study, the results showed that METTL3 and EZH2 were highly expressed in pediatric pneumonia patients and cell models (WI-38), respectively. Besides, downregulation of METTL3 inhibited LPS-induced inflammatory response and cell apoptosis. Then, the fact that METTL3 regulates the JAK2/STAT3 signaling pathway through EZH was proved. Furthermore, downregulation of METTL3 inhibits inflammation and apoptosis through EZH2. Conclusion: This study found that METTL3 promotes inflammation and cell apoptosis in a pediatricpneumonia model by regulating EZH2.

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First person – Xing Du

Journal of Cell Science ◽

10.1242/jcs.257519 ◽

2020 ◽

Vol 133 (23) ◽

pp. jcs257519

Keyword(s):

Molecular Mechanism ◽

Granulosa Cell ◽

Epigenetic Regulation ◽

Cell Apoptosis ◽

Early Career ◽

Female Fertility ◽

First Person ◽

Early Career Researchers ◽

Ovarian Granulosa Cell ◽

Selection Of

ABSTRACTFirst Person is a series of interviews with the first authors of a selection of papers published in Journal of Cell Science, helping early-career researchers promote themselves alongside their papers. Xing Du is first author on ‘SMARCA2 is regulated by NORFA–miR-29c, a novel pathway that controls granulosa cell apoptosis and is related to female fertility’, published in JCS. Xing is a postdoc in the lab of Qifa Li at Nanjing Agricultural University, Jiangsu, China, investigating the genetic mechanism and epigenetic regulation of sow prolificacy, and the molecular mechanism of mammalian ovarian granulosa cell apoptosis.

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