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Inhibition of tumor suppressor p73 by nerve growth factor receptor via chaperone-mediated autophagy

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收录情况： ◇ SCIE ◇ 统计源期刊 ◇ CSCD-C

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单位： [1]Tulane Univ, Tulane Canc Ctr, Dept Biochem & Mol Biol, Sch Med, New Orleans, LA 70112 USA [2]Fudan Univ, Shanghai Canc Ctr, Dept Radiat Oncol, Shanghai Med Sch,Dept Oncol, Shanghai 200032, Peoples R China [3]Baylor Coll Med, Verna & Marrs McLean Dept Biochem & Mol Biol, Houston, TX 77030 USA [4]Fudan Univ, Shanghai Canc Ctr, Dept Radiat Oncol, Shanghai 200032, Peoples R China [5]Fudan Univ, Shanghai Canc Ctr, Inst Biomed Sci, Shanghai 200032, Peoples R China

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关键词： BREAST-CANCER CELLS P53 DEGRADATION GENE PROLIFERATION EXPRESSION NEUROBLASTOMA ACTIVATION DELTA-NP73 MECHANISM

摘要：

The tumor suppressr p73 is a homolog of p53 and is capable of inducing cell cycle arrest and apoptosis. Here, we identify nerve growth factor receptor (NGFR, p75NTR, or CD271) as a novel negative p73 regulator. p73 activates NGFR transcription, which, in turn, promotes p73 degradation in a negative feedback loop. NGFR directly binds to p73 central DNA-binding domain and suppresses p73 transcriptional activity as well as p73-mediated apoptosis in cancer cells. Surprisingly, we uncover a previously unknown mechanism of NGFR-facilitated p73 degradation through the chaperone-mediated autophagy (CMA) pathway. Collectively, our studies demonstrate a new oncogenic function for NGFR in inactivating p73 activity by promoting its degradation through the CMA.

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出版当年[2019]版：

大类 | 2 区生物

小类 | 2 区细胞生物学

最新[2025]版：

大类 | 2 区生物学

小类 | 3 区细胞生物学

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出版当年[2018]版：

Q2 CELL BIOLOGY

最新[2024]版：

Q2 CELL BIOLOGY

影响因子： 5.9 最新[2024版] 6.7 最新五年平均 4.671 出版当年[2018版] 5.856 出版当年五年平均 5.595 出版前一年[2017版] 4 出版后一年[2019版]

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第一作者单位： [1]Tulane Univ, Tulane Canc Ctr, Dept Biochem & Mol Biol, Sch Med, New Orleans, LA 70112 USA

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通讯机构： [1]Tulane Univ, Tulane Canc Ctr, Dept Biochem & Mol Biol, Sch Med, New Orleans, LA 70112 USA [*1]Tulane Univ, Tulane Canc Ctr, Dept Biochem & Mol Biol, Sch Med, New Orleans, LA 70112 USA

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