Academic Journal

Ion channel TRPML2 (MCOLN2) promotes ovarian cancer metastasis and chemoresistance.

Λεπτομέρειες βιβλιογραφικής εγγραφής
Τίτλος: Ion channel TRPML2 (MCOLN2) promotes ovarian cancer metastasis and chemoresistance.
Συγγραφείς: Yang S; Department of Obstetrics and Gynecology, Affiliated Hospital of Jiangnan University, Wuxi, Jiangsu, China. Electronic address: yangsz1986@126.cim., Lei Z; School of Biomedical Sciences, Heart and Vascular Institute and Li Ka Shing Institute of Health Sciences, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong, China., Yao X; School of Biomedical Sciences, Heart and Vascular Institute and Li Ka Shing Institute of Health Sciences, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong, China., Yu J; Department of Obstetrics and Gynecology, Affiliated Hospital of Jiangnan University, Wuxi, Jiangsu, China.
Πηγή: Biochemical and biophysical research communications [Biochem Biophys Res Commun] 2026 Sep 17; Vol. 831, pp. 154288. Date of Electronic Publication: 2026 Jul 14.
Τύπος έκδοσης: Journal Article
Γλώσσα: English
Στοιχεία περιοδικού: Publisher: Elsevier Country of Publication: United States NLM ID: 0372516 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1090-2104 (Electronic) Linking ISSN: 0006291X NLM ISO Abbreviation: Biochem Biophys Res Commun Subsets: MEDLINE
Imprint Name(s): Publication: <2002- >: San Diego, CA : Elsevier
Original Publication: New York, Academic Press.
Ιατρικοί όροι (MeSH): Ovarian Neoplasms*/pathology , Ovarian Neoplasms*/metabolism , Ovarian Neoplasms*/drug therapy , Ovarian Neoplasms*/genetics , Transient Receptor Potential Channels*/metabolism , Transient Receptor Potential Channels*/genetics , Drug Resistance, Neoplasm*, Cell Movement/drug effects ; Carboplatin/pharmacology ; Antineoplastic Agents/pharmacology ; Cell Proliferation/drug effects ; Female ; Humans ; Cell Line, Tumor ; Neoplasm Metastasis ; Gene Expression Regulation, Neoplastic
Περίληψη: Background: Ovarian cancer, with metastasis and chemoresistance being the major obstacles to successful treatment, is a leading cause of death among gynecological malignancies. Identifying new molecular targets and understanding the underlying mechanisms of metastasis and chemoresistance are pressing issues in ovarian cancer therapy. Emerging evidence suggests that an endolysosomal Ca2+-permeable channel TRPML2 may contribute to cancer progression. However, its exact role and associated underlying mechanisms in ovarian cancer remain largely unknown.
Methods: TRPML2 expression was studied by tissue and cellular immunostaining and western blots. The functional role of TRPML2 in cancer was assessed by cell viability assay, colony-formation assay, wound-healing assay and transwell assay. The resistance to carboplatin-induced cytotoxic effects was evaluated by Cell Counting Kit-8.
Results: The TRPML2 expression is elevated in ovarian cancer cell lines and ovarian tumor tissues with high expression predicting a poor prognosis in ovarian cancer. TRPML2 knockdown with siRNA markedly reduced the proliferation of ovarian cancer cells, decreased the colony formation and migration, and increased the sensitivity of ovarian cancer cells to a chemoresistant drug carboplatin.
Conclusion: In summary, TRPML2 is critically involved in ovarian cancer progression and chemoresistance to carboplatin. Our study highlights an exciting possibility of targeting TRPML2 as a potential therapeutic option.
(Copyright © 2026 Elsevier Inc. All rights reserved.)
Competing Interests: Declaration of competing interest The authors declare no competing interests in potential conflicts of interest include employment, consultancies, stock ownership, honoraria, paid expert testimony, patent applications/registrations, and grants or other funding.
Contributed Indexing: Keywords: Chemoresistance; Ion channel; MCOLN2; Ovarian cancer metastasis; TRPML2
Substance Nomenclature: 0 (Transient Receptor Potential Channels)
0 (Mcoln2 protein, human)
BG3F62OND5 (Carboplatin)
0 (Antineoplastic Agents)
Entry Date(s): Date Created: 20260722 Date Completed: 20260812 Latest Revision: 20260812
Update Code: 20260813
DOI: 10.1016/j.bbrc.2026.154288
PMID: 42485795
Βάση Δεδομένων: MEDLINE
Περιγραφή
ISSN:1090-2104
DOI:10.1016/j.bbrc.2026.154288