Targeting centromere protein M represses cell growth and mobility via inactivating AKT pathway but less affects BRAF inhibitor sensitivity in cutaneous melanoma.

Shujie Ruan, Zhechen Zhu, Binlin Luo, Youzhi Tang, Wei Yan, Jingping Shi

Abstract read

In one paragraph

Article in Naunyn-Schmiedeberg's archives of pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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5 · Who and what money

Authors and funding

6 authors.

Shujie RuanDepartment of Plastic and Burn Surgery, The First Affiliated Hospital with Nanjing Medical University, Jiangsu Province Hospital, No. 300 Guangzhou Road, Nanjing, 210029, Jiangsu Province, China. rsj_njmu@163.com.

Zhechen ZhuDepartment of Plastic and Burn Surgery, The First Affiliated Hospital with Nanjing Medical University, Jiangsu Province Hospital, No. 300 Guangzhou Road, Nanjing, 210029, Jiangsu Province, China.

Binlin LuoDepartment of Plastic and Burn Surgery, The First Affiliated Hospital with Nanjing Medical University, Jiangsu Province Hospital, No. 300 Guangzhou Road, Nanjing, 210029, Jiangsu Province, China.

Youzhi TangDepartment of Plastic and Burn Surgery, The First Affiliated Hospital with Nanjing Medical University, Jiangsu Province Hospital, No. 300 Guangzhou Road, Nanjing, 210029, Jiangsu Province, China.

Wei YanDepartment of Plastic and Burn Surgery, The First Affiliated Hospital with Nanjing Medical University, Jiangsu Province Hospital, No. 300 Guangzhou Road, Nanjing, 210029, Jiangsu Province, China.

Jingping ShiDepartment of Plastic and Burn Surgery, The First Affiliated Hospital with Nanjing Medical University, Jiangsu Province Hospital, No. 300 Guangzhou Road, Nanjing, 210029, Jiangsu Province, China. drshi_njmu@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Centromere protein M (CENPM) promotes oncogenesis and serves as a prognostic biomarker in some cancers, but its implication in cutaneous melanoma is not clear. This study aimed to investigate the effect of targeting CENPM on cell proliferation, colony ability, apoptosis, invasion, migration, and BRAF inhibitor sensitivity, and its modification on Wnt/β-catenin, AKT, and P53 pathways in cutaneous melanoma. Cutaneous melanoma cell lines (A375 and SK-MEL-28) were transfected by CENPM siRNA (si-CENPM), followed by detections and treatment of various concentrations of dabrafenib and vemurafenib. Afterwards, 740Y-P (AKT activator) was added with or without si-CENPM transfection followed by detections. Gene Expression Profiling Interactive Analysis (GEPIA) public database was applied for clinical analysis. si-CENPM reduced cell proliferation, invasive cells and cell migration rate, but induced cell apoptosis rate in A375 and SK-MEL-28 cells. Meanwhile, si-CENPM decreased colony ability in A375 cells but didn't change colony ability in SK-MEL-28 cells. However, si-CENPM did not change cell viability under each concentration or IC

Indexed as

Antineoplastic AgentsChromosomal Proteins, Non-HistoneMelanomaProtein Kinase InhibitorsProto-Oncogene Proteins B-rafProto-Oncogene Proteins c-aktSkin NeoplasmsApoptosisCell Line, TumorCell MovementCell ProliferationCutaneous Malignant MelanomaHumansImidazolesOximesVemurafenibAntineoplastic AgentsBRAF protein, humanChromosomal Proteins, Non-HistonedabrafenibImidazolesOximesProtein Kinase InhibitorsProto-Oncogene Proteins B-rafProto-Oncogene Proteins c-aktVemurafenibAKT pathwayBRAF inhibitor sensitivityCellular functionsCentromere protein MCutaneous melanoma

Identifiers

PMID41324664

DOI10.1002/ctm2.70182

What Socratic holds

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.