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      NRBF2 regulates the chemoresistance of small cell lung cancer by interacting with the P62 protein in the autophagy process

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          Summary

          Reversing chemotherapy resistance in small cell lung cancer (SCLC) is crucial to improve patient prognosis. The present study aims to investigate the underlying mechanisms in SCLC chemoresistance. We see that nuclear receptor binding factor 2 (NRBF2) is a poor prognostic factor in SCLC. The effects of NRBF2 on chemoresistance were determined in SCLC. The underlying molecular mechanisms of NRBF2 in the autophagy process in SCLC were examined. NRBF2 positively regulated autophagy, leading to drug resistance in SCLC. The MIT domain of NRBF2 directly interacted with the PB1 domain of P62. This interaction increased autophagic P62 body formation, revealing the regulatory role of NRBF2 in autophagy. Notably, NRBF2 was directly modulated by the transcription factor XRCC6. The MIT domain of NRBF2 interacts with the PB1 domain of P62 to regulate the autophagy process, resulting in SCLC chemoresistance. NRBF2 is likely a useful chemotherapy response marker and therapeutic target in SCLC.

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          Highlights

          • •

            NRBF2 promoted the chemoresistance of SCLC in vitro and in vivo

          • •

            The chemoresistance induced by NRBF2 was mediated via autophagy in SCLC

          • •

            NRBF2 interacting with P62 contributed to autophagic P62 bodies' formation

          • •

            NRBF2 was regulated by XRCC6 via direct binding to the NRBF2 gene promoter

          Abstract

          Cell biology; Cancer

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          Most cited references40

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          Colorectal cancer statistics, 2017.

          Rebecca Siegel, Kimberly D Miller, Stacey Fedewa … (2017)
          Colorectal cancer (CRC) is one of the most common malignancies in the United States. Every 3 years, the American Cancer Society provides an update of CRC incidence, survival, and mortality rates and trends. Incidence data through 2013 were provided by the Surveillance, Epidemiology, and End Results program, the National Program of Cancer Registries, and the North American Association of Central Cancer Registries. Mortality data through 2014 were provided by the National Center for Health Statistics. CRC incidence rates are highest in Alaska Natives and blacks and lowest in Asian/Pacific Islanders, and they are 30% to 40% higher in men than in women. Recent temporal patterns are generally similar by race and sex, but differ by age. Between 2000 and 2013, incidence rates in adults aged ≥50 years declined by 32%, with the drop largest for distal tumors in people aged ≥65 years (incidence rate ratio [IRR], 0.50; 95% confidence interval [95% CI], 0.48-0.52) and smallest for rectal tumors in ages 50 to 64 years (male IRR, 0.91; 95% CI, 0.85-0.96; female IRR, 1.00; 95% CI, 0.93-1.08). Overall CRC incidence in individuals ages ≥50 years declined from 2009 to 2013 in every state except Arkansas, with the decrease exceeding 5% annually in 7 states; however, rectal tumor incidence in those ages 50 to 64 years was stable in most states. Among adults aged <50 years, CRC incidence rates increased by 22% from 2000 to 2013, driven solely by tumors in the distal colon (IRR, 1.24; 95% CI, 1.13-1.35) and rectum (IRR, 1.22; 95% CI, 1.13-1.31). Similar to incidence patterns, CRC death rates decreased by 34% among individuals aged ≥50 years during 2000 through 2014, but increased by 13% in those aged <50 years. Progress against CRC can be accelerated by increasing initiation of screening at age 50 years (average risk) or earlier (eg, family history of CRC/advanced adenomas) and eliminating disparities in high-quality treatment. In addition, research is needed to elucidate causes for increasing CRC in young adults. CA Cancer J Clin 2017. © 2017 American Cancer Society. CA Cancer J Clin 2017;67:177-193. © 2017 American Cancer Society.
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            Autophagy and multidrug resistance in cancer

            Ying-Jie Li, Yu-He Lei, Nan Yao … (2017)
            Multidrug resistance (MDR) occurs frequently after long-term chemotherapy, resulting in refractory cancer and tumor recurrence. Therefore, combatting MDR is an important issue. Autophagy, a self-degradative system, universally arises during the treatment of sensitive and MDR cancer. Autophagy can be a double-edged sword for MDR tumors: it participates in the development of MDR and protects cancer cells from chemotherapeutics but can also kill MDR cancer cells in which apoptosis pathways are inactive. Autophagy induced by anticancer drugs could also activate apoptosis signaling pathways in MDR cells, facilitating MDR reversal. Therefore, research on the regulation of autophagy to combat MDR is expanding and is becoming increasingly important. We summarize advanced studies of autophagy in MDR tumors, including the variable role of autophagy in MDR cancer cells.
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              Unravelling the biology of SCLC: implications for therapy

              Joshua Sabari, Benjamin H Lok, James H. Laird … (2017)
              For three decades, the treatment of small-cell lung cancer (SCLC) has remained essentially unchanged, and patient outcomes remain dismal. In the past 5 years, however, advances in our understanding of the disease, at the molecular level, have resulted in the development of new therapeutic strategies, encompassing immunotherapies and novel molecularly targeted agents. Herein, authors review the breakthroughs that hold the promise to improve SCLC outcomes.
              Article 0 comments Cited 192 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Jian Zhang
                Hai-Hong Wang
                Ting Wei
                Journal
                Journal ID (nlm-ta): iScience
                Journal ID (iso-abbrev): iScience
                Title: iScience
                Publisher: Elsevier
                ISSN (Electronic): 2589-0042
                Publication date PMC-release: 26 May 2022
                Publication date Collection: 17 June 2022
                Publication date (Electronic): 26 May 2022
                Volume: 25
                Issue: 6
                Electronic Location Identifier: 104471
                Affiliations
                [1 ]Department of Oncology, Zhujiang Hospital, Southern Medical University, 253 Industrial Avenue, Guangzhou 510282, Guangdong, People’s Republic of China
                [2 ]Department of Medical Oncology, Sun Yat-Sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangzhou 510282, Guangdong, People’s Republic of China
                [3 ]Department of Rehabilitation, The Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai 519000, Guangdong, People’s Republic of China
                [4 ]The Second School of Clinical Medicine, Southern Medical University, Guangzhou 510515, Guangdong, People’s Republic of China
                [5 ]Department of Neurosurgery, Xiangya Hospital, Central South University, Changsha 410008, Hunan, People’s Republic of China
                [6 ]Department of Histology and Embryology, School of Basic Medical Sciences, Southern Medical University, Guangzhou 510515, Guangdong, People’s Republic of China
                Author notes
                [∗ ]Corresponding author zhangjian@ 123456i.smu.edu.cn
                [∗∗ ]Corresponding author haihwang@ 123456163.com
                [∗∗∗ ]Corresponding author weitingyouyou@ 123456qq.com
                [7]

                These authors contributed equally

                [8]

                Lead contact

                Article
                Publisher Item ID: S2589-0042(22)00742-8 Publisher ID: 104471
                DOI: 10.1016/j.isci.2022.104471
                PMC ID: 9194155
                PubMed ID: 35712081
                SO-VID: 64dc7c93-5577-4cba-a59e-5ab51eecdf33
                Copyright © © 2022.
                License:

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                Date received : 4 November 2021
                Date revision received : 22 February 2022
                Date accepted : 20 May 2022
                Categories
                Subject: Article

                Keywords: cell biology,cancer
                Data availability:
                Keywords: cell biology, cancer

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