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      The oncogene MYBL2 promotes the malignant phenotype and suppresses apoptosis through hedgehog signaling pathway in clear cell renal cell carcinoma

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          Abstract

          Multiple cancers have been associated with MYB-related protein B (MYBL2), its involvement in clear cell renal cell carcinoma (ccRCC) has yet to be demonstrated. Our study revealed a significant upregulation of MYBL2 in ccRCC tissues, correlating with clinicopathological features and patient prognosis. Increased MYBL2 expression promoted cell proliferation and suppressed apoptosis. RNA-seq analysis unveiled a reduction in smoothened (SMO) expression upon MYBL2 silencing. However, luciferase and chromatin immunoprecipitation (ChIP) assays demonstrated MYBL2's positive regulation of SMO expression by directly targeting the SMO promoter. Reintroduction of SMO expression in MYBL2-knocked down cells partially restored cell proliferation and mitigated apoptosis inhibition. Overall, these results indicate that MYBL2 facilitates ccRCC progression by enhancing SMO expression, suggesting its potential as an intriguing drug target for ccRCC therapy.

          Highlights

          • •

            Enhanced MYBL2 levels are linked to advanced progression in ccRCC patients.

          • •

            MYBL2 accelerates the proliferation and suppresses apoptosis of ccRCC cells.

          • •

            MYBL2 regulated the HH signaling pathway.

          • •

            SMO can partially restore the malignancy traits of MYBL2-inhibited cells.

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          Most cited references41

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          Cancer statistics, 2022

          Rebecca Siegel, Kimberly D Miller, Hannah Fuchs … (2022)
          Each year, the American Cancer Society estimates the numbers of new cancer cases and deaths in the United States and compiles the most recent data on population-based cancer occurrence and outcomes. Incidence data (through 2018) were collected 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 2019) were collected by the National Center for Health Statistics. In 2022, 1,918,030 new cancer cases and 609,360 cancer deaths are projected to occur in the United States, including approximately 350 deaths per day from lung cancer, the leading cause of cancer death. Incidence during 2014 through 2018 continued a slow increase for female breast cancer (by 0.5% annually) and remained stable for prostate cancer, despite a 4% to 6% annual increase for advanced disease since 2011. Consequently, the proportion of prostate cancer diagnosed at a distant stage increased from 3.9% to 8.2% over the past decade. In contrast, lung cancer incidence continued to decline steeply for advanced disease while rates for localized-stage increased suddenly by 4.5% annually, contributing to gains both in the proportion of localized-stage diagnoses (from 17% in 2004 to 28% in 2018) and 3-year relative survival (from 21% to 31%). Mortality patterns reflect incidence trends, with declines accelerating for lung cancer, slowing for breast cancer, and stabilizing for prostate cancer. In summary, progress has stagnated for breast and prostate cancers but strengthened for lung cancer, coinciding with changes in medical practice related to cancer screening and/or treatment. More targeted cancer control interventions and investment in improved early detection and treatment would facilitate reductions in cancer mortality.
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            Epidemiology of Renal Cell Carcinoma

            Umberto Capitanio, Karim Bensalah, Axel Bex … (2019)
            Despite the improvement in renal cell carcinoma (RCC) diagnosis and management observed during the last 2 decades, RCC remains one of the most lethal urological malignancies. With the expansion of routine imaging for many disorders, an increasing number of patients who harbour RCC are identified incidentally.
            Article 0 comments Cited 460 times – based on 0 reviews     Review now
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              The mechanisms of Hedgehog signalling and its roles in development and disease.

              James Briscoe, P Thérond (2013)
              The cloning of the founding member of the Hedgehog (HH) family of secreted proteins two decades ago inaugurated a field that has diversified to encompass embryonic development, stem cell biology and tissue homeostasis. Interest in HH signalling increased when the pathway was implicated in several cancers and congenital syndromes. The mechanism of HH signalling is complex and remains incompletely understood. Nevertheless, studies have revealed novel biological insights into this system, including the function of HH lipidation in the secretion and transport of this ligand and details of the signal transduction pathway, which involves Patched 1, Smoothened and GLI proteins (Cubitus interruptus in Drosophila melanogaster), as well as, in vertebrates, primary cilia.
              Article 0 comments Cited 309 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Jie dong
                He Xiao
                Journal
                Journal ID (nlm-ta): Heliyon
                Journal ID (iso-abbrev): Heliyon
                Title: Heliyon
                Publisher: Elsevier
                ISSN (Electronic): 2405-8440
                Publication date PMC-release: 11 March 2024
                Publication date Collection: 30 March 2024
                Publication date (Electronic): 11 March 2024
                Volume: 10
                Issue: 6
                Electronic Location Identifier: e27772
                Affiliations
                [1]Department of Urology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Dongcheng, Beijing, 100000, China
                Author notes
                [* ]Corresponding author. Department of Urology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Dongcheng, Beijing 10000, China. pumchdongjie@ 123456163.com
                [** ]Corresponding author. xiaoh@ 123456pumch.cn
                [1]

                These authors contributed equally to this work.

                Article
                Publisher Item ID: S2405-8440(24)03803-9 Publisher ID: e27772
                DOI: 10.1016/j.heliyon.2024.e27772
                PMC ID: 10950673
                PubMed ID: 38510035
                SO-VID: 372c681c-07f1-45eb-85fc-b4c4d36cd39e
                Copyright © © 2024 The Authors
                License:

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

                History
                Date received : 27 October 2023
                Date revision received : 6 March 2024
                Date accepted : 6 March 2024
                Categories
                Subject: Research Article

                Keywords: ccrcc,mybl2,proliferation,apoptosis,smo
                Data availability:
                Keywords: ccrcc, mybl2, proliferation, apoptosis, smo

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