ArticleInternational journal of oncology2018
MORC2, a novel oncogene, is upregulated in liver cancer and contributes to proliferation, metastasis and chemoresistance.
Article in International journal of oncology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 41 citations in OpenAlex.
- Glutamine: fructose-6-phosphate amidotransferase (GFAT) in the pathology of diseases: a review.Cell death discovery · 2025Review
- MORC2 is a phosphorylation-dependent DNA compaction machine.Nature communications · 2025Article
- Regulation of MORC-1 is key to the CSR-1-mediated germline gene licensing mechanism inScience advances · 2025Article
- Lactic acid metabolism: gynecological cancer's Achilles' heel.Discover oncology · 2025Review
- CRISPR/Cas9 system: a novel approach to overcome chemotherapy and radiotherapy resistance in cancer.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Bioinformatics Analysis Reveals Microrchidia Family Genes as the Prognostic and Therapeutic Markers for Colorectal Cancer.Endocrine, metabolic & immune disorders drug targets · 2025Article
- Netrin-1 and UNC5B Cooperate with Integrins to Mediate YAP-Driven Cytostasis.Cancer research communications · 2024Article
- Emerging roles of the chromatin remodeler MORC2 in cancer metabolism.Medical oncology (Northwood, London, England) · 2024Review
- Oncogenic MORC2 in cancer development and beyond.Genes & diseases · 2024Review
- TheNeural regeneration research · 2024Article
- Novel Insights into the Role of Chromatin Remodeler MORC2 in Cancer.Biomolecules · 2023Review
- Identifying Suitable Reference Gene Candidates for Quantification of DNA Damage-Induced Cellular Responses in Human U2OS Cell Culture System.Biomolecules · 2023Article
- Review
- MORC4 plays a tumor-promoting role in colorectal cancer via regulating PCGF1/CDKN1A axis in vitro and in vivo.Cancer gene therapy · 2023Article
- MORC2 and MAX contributes to the expression of glycolytic enzymes, breast cancer cell proliferation and migration.Medical oncology (Northwood, London, England) · 2023Article
- High Expression of MORC2 is Associated with Poor Clinical Outcomes and Immune Infiltrates in Colon Adenocarcinoma.International journal of general medicine · 2023Article
- Inhibition of MORC2 Mediates HDAC4 to Promote Cellular Senescence through p53/p21 Signaling Axis.Molecules (Basel, Switzerland) · 2022Article
- MORC2/β-catenin signaling axis promotes proliferation and migration of breast cancer cells.Medical oncology (Northwood, London, England) · 2022Article
- HSP90 N-terminal inhibitors target oncoprotein MORC2 for autophagic degradation and suppress MORC2-driven breast cancer progression.Clinical and translational medicine · 2022Article
- O-GlcNAcylation of MORC2 at threonine 556 by OGT couples TGF-β signaling to breast cancer progression.Cell death and differentiation · 2022Article
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Authors and funding
9 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Microrchidia 2 (MORC2) is important in DNA damage repair and lipogenesis, however, the clinical and functional role of MORC2 in liver cancer remains to be fully elucidated. The aim the present study was to clarify the role of MORC2 in liver cancer. Expression profile analysis, immunohistochemical staining, reverse transcription-quantitative polymerase chain reaction analysis and western blot analysis were performed to evaluate the levels of MORC2 in liver cancer patient specimens and cell lines; subsequently the expression of MORC2 was suppressed or increased in liver cancer cells and the effects of MORC2 on the cancerous transformation of liver cancer cells were examined in vitro and in vivo. MORC2 was upregulated in liver cancer tissues, and the upregulation was associated with certain clinicopathologic features of patients with liver cancer. MORC2 knockdown caused marked inhibition of liver cancer cell proliferation and clonogenicity, whereas the overexpression of MORC2 substantially promoted liver cancer cell proliferation. In addition, the knockdown of MORC2 inhibited the migratory and invasive ability of liver cancer cells, whereas increased migration and invasion rates were observed in cells with ectopic expression of MORC2. In a model of nude mice, the overexpression of MORC2 promoted tumorigenicity and markedly enhanced pulmonary metastasis of liver cancer. Furthermore, MORC2 regulated apoptosis and its expression level had an effect on the sensitivity of liver cancer cells to doxorubicin, 5-fluorouracil and cisplatin. Mechanically, MORC2 modulated the mitochondrial apoptotic pathway, possibly in a p53-dependent manner, and its dysregulation also resulted in the abnormal activation of the Hippo pathway. For the first time, to the best of our knowledge, the present study confirmed that MORC2 was a novel oncogene in liver cancer. These results provide useful insight into the mechanism underlying the tumorigenesis and progression of liver cancer, and offers clues into potential novel liver cancer therapies.
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