Yanping Shi

Guiyang Medical University

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Congwei Jia

Peking Union Medical College Hospital

Joanna Zawacka‐Pankau

Karolinska Institutet

K. Meller

Gdańsk Medical University

Yingchun Zhang

University of Science and Technology Beijing

Aleksandra Królicka

University of Gdańsk

Chao Ma

Wuhan University

Ye Zeng

Affiliated Hospital of Southwest Medical University

Alberto Inga

University of Trento

Lihua Zhang

Dalian Institute of Chemical Physics

M. Lion

University of Liège

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Peking Union Medical College Hospital

Chinese Academy of Medical Sciences & Peking Union Medical College

Gdańsk Medical University

Karolinska Institutet

Guiyang Medical University

Southwest University

University of Gdańsk

Sichuan University

University of Trento

West China Second University Hospital of Sichuan University

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Targeting ENPP1 depletion may be a promising therapeutic strategy for treating oral squamous cell carcinoma via cytotoxic autophagy‐related apoptosis

The FASEB Journal (2024)

Chao Ma Jizhi Zhao L. Zhou Congwei Jia Yanping Shi

Abstract ENPP1 depletion closely related with modulation immunotherapy of several types of cancer. However, the role of ENPP1 correlation with autophagy in oral squamous cell carcinoma (OSCC) pathogenesis remain unknown. In this study, effects of ENPP1 on OSCC cells in vitro were examined by cell proliferation assay, transwell chamber assay, flow cytometry analysis and shRNA technique. Cellular key proteins related to cell autophagy and apoptosis were evaluated by Western blot and immunofluorescent staining. Moreover, functions of ENPP1 on OSCC process were observed in nude mouse model. We reported that overexpression of ENPP1 promote the growth of OSCC cell xenografts in nude mouse model. In contrast, ENPP1 downregulation significantly inhibits OSCC cancer growth and induces apoptosis both in vitro and in vivo, which are preceded by cytotoxic autophagy. ENPP1downregulation induces a robust accumulation of autophagosomes, increases LC3B‐II and decreases SQSTM1/p62 in ENPP1‐shRNA‐treated cells and xenografts. Mechanistic studies show that ENPP1 downregulation increases PRKAA1 phosphorylation leading to ULK1 activation. AMPK‐inhibition abrogates ENPP1 downregulation‐induced ULK1‐activation, LC3B‐turnover and SQSTM1/p62‐degradation while AMPK‐activation potentiates it's effects. Collectively, these data uncover that ENPP1 downregulation induces autophagic cell death in OSCC cancer, which may provide a potential therapeutic target for the treatment of OSCC.

10.1096/fj.202301835r

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Correction to: JNK–NQO1 axis drives TAp73-mediated tumor suppression upon oxidative and proteasomal stress

Cell Death and Disease (2018)

Anna Kostecka Alicja Sznarkowska K. Meller Pilar Acedo Yanping Shi

Following publication of their Article JNK-NQO1 axis drives TAp73-mediated tumor suppression upon oxidative and proteasomal stress. Cell Death Dis. 2014, 5:e1484, the authors noted a mistake in Figure 2b, in that, the wells of the crystal violet plates showing growth inhibition induced by withaferin A in HCT 116TP53-/- cells were erroneously duplicated for 1 and 2.5 μM WA. The correct wells for 2.5 μM WA are now included in new figure 2b (please see attached file).

Mistake

10.1038/s41419-018-0655-1

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Antimicrobial peptide Mt 5 inhibits human hepatocellular carcinoma cell HepG2 proliferation

Biochemical and Biophysical Research Communications (2024)

Yanping Shi Ye Zeng Ruifeng Zuo Sheng‐Hua Wu Lihua Zhang

10.1016/j.bbrc.2024.151126

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