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      FUNDC2, a mitochondrial outer membrane protein, mediates triple-negative breast cancer progression via the AKT/GSK3β/GLI1 pathway : FUNDC2 mediates TNBC progression via the AKT/GSK3β/GLI1 pathway

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          Abstract

          Triple-negative breast cancer (TNBC) lacks effective therapeutic targets and has a poor prognosis, easy recurrence and metastasis. It is urgent and important to explore TNBC treatment targets. Through mass spectrometry combined with qRT-PCR validation in luminal A cells and TNBC cells, high-content screening and clinical sample analysis, FUNDC2 was discovered as a novel target. The function of the outer mitochondrial membrane protein FUNDC2 in breast cancer is still unclear. In this study, we find that FUNDC2 expression in TNBC tissues is significantly higher than that in luminal subtype breast cancer tissues. FUNDC2 silencing in TNBC cells significantly reduces cell proliferation, migration and invasion. As demonstrated in vivo using subcutaneous tumor xenografts in mice, FUNDC2 suppression significantly inhibits tumor growth. The underlying mechanism might be mediated by inactivating its downstream signal AKT/GSK3β and GLI1, a key factor of the Hedgehog signaling pathway. Therefore, FUNDC2 may promote TNBC progression and provide a therapeutic target for treating TNBC.

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          Global cancer statistics 2020: GLOBOCAN estimates of incidence and mortality worldwide for 36 cancers in 185 countries

          Hyuna Sung, Jacques Ferlay, Rebecca Siegel … (2021)
          This article provides an update on the global cancer burden using the GLOBOCAN 2020 estimates of cancer incidence and mortality produced by the International Agency for Research on Cancer. Worldwide, an estimated 19.3 million new cancer cases (18.1 million excluding nonmelanoma skin cancer) and almost 10.0 million cancer deaths (9.9 million excluding nonmelanoma skin cancer) occurred in 2020. Female breast cancer has surpassed lung cancer as the most commonly diagnosed cancer, with an estimated 2.3 million new cases (11.7%), followed by lung (11.4%), colorectal (10.0 %), prostate (7.3%), and stomach (5.6%) cancers. Lung cancer remained the leading cause of cancer death, with an estimated 1.8 million deaths (18%), followed by colorectal (9.4%), liver (8.3%), stomach (7.7%), and female breast (6.9%) cancers. Overall incidence was from 2-fold to 3-fold higher in transitioned versus transitioning countries for both sexes, whereas mortality varied <2-fold for men and little for women. Death rates for female breast and cervical cancers, however, were considerably higher in transitioning versus transitioned countries (15.0 vs 12.8 per 100,000 and 12.4 vs 5.2 per 100,000, respectively). The global cancer burden is expected to be 28.4 million cases in 2040, a 47% rise from 2020, with a larger increase in transitioning (64% to 95%) versus transitioned (32% to 56%) countries due to demographic changes, although this may be further exacerbated by increasing risk factors associated with globalization and a growing economy. Efforts to build a sustainable infrastructure for the dissemination of cancer prevention measures and provision of cancer care in transitioning countries is critical for global cancer control.
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            Mitochondrial outer-membrane protein FUNDC1 mediates hypoxia-induced mitophagy in mammalian cells.

            Lei Liu, Du Feng, Guo Chen … (2012)
            Accumulating evidence has shown that dysfunctional mitochondria can be selectively removed by mitophagy. Dysregulation of mitophagy is implicated in the development of neurodegenerative disease and metabolic disorders. How individual mitochondria are recognized for removal and how this process is regulated remain poorly understood. Here we report that FUNDC1, an integral mitochondrial outer-membrane protein, is a receptor for hypoxia-induced mitophagy. FUNDC1 interacted with LC3 through its typical LC3-binding motif Y(18)xxL(21), and mutation of the LC3-interaction region impaired its interaction with LC3 and the subsequent induction of mitophagy. Knockdown of endogenous FUNDC1 significantly prevented hypoxia-induced mitophagy, which could be reversed by the expression of wild-type FUNDC1, but not LC3-interaction-deficient FUNDC1 mutants. Mechanistic studies further revealed that hypoxia induced dephosphorylation of FUNDC1 and enhanced its interaction with LC3 for selective mitophagy. Our findings thus offer insights into mitochondrial quality control in mammalian cells.
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              The Landscape of Targeted Therapies in TNBC

              Elena Vagia, Devalingam Mahalingam, Massimo Cristofanilli (2020)
              Triple negative breast cancer (TNBC) constitutes the most aggressive molecular subtype among breast tumors. Despite progress on the underlying tumor biology, clinical outcomes for TNBC unfortunately remain poor. The median overall survival for patients with metastatic TNBC is approximately eighteen months. Chemotherapy is the mainstay of treatment while there is a growing body of evidence that targeted therapies may be on the horizon with poly-ADP-ribose polymerase (PARP) and immune check-point inhibitors already established in the treatment paradigm of TNBC. A large number of novel therapeutic agents are being evaluated for their efficacy in TNBC. As novel therapeutics are now incorporated into clinical practice, it is clear that tumor heterogeneity and clonal evolution can result to de novo or acquired treatment resistance. As precision medicine and next generation sequencing is part of cancer diagnostics, tailored treatment approaches based on the expression of molecular markers are currently being implemented in clinical practice and clinical trial design. The scope of this review is to highlight the most relevant current knowledge regarding underlying molecular profile of TNBC and its potential application in clinical practice.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Acta Biochim Biophys Sin (Shanghai)
                Journal ID (iso-abbrev): Acta Biochim Biophys Sin (Shanghai)
                Journal ID (publisher-id): ABBS
                Title: Acta Biochimica et Biophysica Sinica
                Publisher: Oxford University Press
                ISSN (Print): 1672-9145
                ISSN (Electronic): 1745-7270
                Publication date (Electronic): 11 September 2023
                Publication date Collection: 25 November 2023
                Publication date PMC-release: 11 September 2023
                Volume: 55
                Issue: 11
                Pages: 1770-1783
                Affiliations
                [1 ] orgnameThe First Affiliated Hospital orgnameCancer Research Institute orgnameHengyang Medical School orgnameUniversity of South China Hengyang 421001 China
                [2The ] orgnameNanhua Affiliated Hospital orgnameDepartment of Spine Surgery orgnameHengyang Medical School orgnameUniversity of South China Hengyang 421001 China
                Author notes
                Correspondence address. Tel: +86-734-8279476; (Y.S.) / Tel: +86-734-8279382; E-mail: (X.Z.) shenyingying@nhfyyy.comzuxuyu0108@hotmail.com
                Article
                DOI: 10.3724/abbs.2023142
                PMC ID: 10679879
                PubMed ID: 37700593
                SO-VID: b254a288-ba1e-48ba-9e84-50cf2d06620d
                Copyright © © The Author(s) 2021.
                License:

                0

                This is an open access article distributed under the terms of the Creative Commons Attribution Licence (https://creativecommons.org/licenses/by/4.0/).

                History
                Date received : 6 April 2023
                Date accepted : 12 May 2023
                Funding
                Funded by: the grants from the National Natural Science Foundation of China
                Award ID: No.
                Award ID: 81972487
                Funded by: the Natural Science Foundation of Hunan Province
                Award ID: Nos.
                Award ID: 2022JJ70038
                Award ID: 2021JJ20039
                Award ID: 2020JJ4551
                Funded by: the Health Commission of Hunan Province
                Award ID: Nos.
                Award ID: 20201926
                Award ID: 202104070680
                Funded by: and the Education Department of Hunan Province
                Award ID: No.
                Award ID: 20C1592
                This work was supported by the grants from the National Natural Science Foundation of China (No. 81972487), the Natural Science Foundation of Hunan Province (Nos. 2022JJ70038, 2021JJ20039, and 2020JJ4551), the Health Commission of Hunan Province (Nos. 20201926 and 202104070680), and the Education Department of Hunan Province (No. 20C1592).
                Categories
                Subject: Research Article
                Custom metadata
                Citation L Yin, R Cao, Z Liu, G Luo, Y Li, X Zhou, X Chen, et al. FUNDC2, a mitochondrial outer membrane protein, mediates triple-negative breast cancer progression via the AKT/GSK3β/GLI1 pathway. Acta Biochim Biophys Sin, 2023, Vol.: fpage–lpage, https://doi.org/10.3724/abbs.2023142
                Crossmark 2023/9/6 14:36:44
                AuthorMark L Yin
                AuthorMarkCite L Yin, R Cao, Z Liu, G Luo, Y Li, X Zhou, X Chen, et al.
                article-title FUNDC2, a mitochondrial outer membrane protein, mediates triple-negative breast cancer progression via the AKT/GSK3β/GLI1 pathway

                Keywords: fundc2,gli1,triple-negative breast cancer (tnbc),therapeutic target
                Data availability:
                Keywords: fundc2, gli1, triple-negative breast cancer (tnbc), therapeutic target

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