CENPM

Last update 08 May 2025

Basic Info

Synonyms

C22orf18, CENP-M, CENPM

+ [6]

Introduction

Component of the CENPA-NAC (nucleosome-associated) complex, a complex that plays a central role in assembly of kinetochore proteins, mitotic progression and chromosome segregation. The CENPA-NAC complex recruits the CENPA-CAD (nucleosome distal) complex and may be involved in incorporation of newly synthesized CENPA into centromeres.

100 Clinical Results associated with CENPM

100 Translational Medicine associated with CENPM

0 Patents (Medical) associated with CENPM

Literatures (Medical) associated with CENPM

01 Jan 2025·Clinical and Translational Medicine

Identification of CENPM as a key gene driving adrenocortical carcinoma metastasis via physical interaction with immune checkpoint ligand FGL1

Article

Author: Zou, Cunru ; Zhang, Yu ; Liu, Chengyue ; Lin, Congjie ; Yan, Qiupeng ; Li, Yaxin ; Gao, Guojun ; Hou, Jiangping ; Chen, Hao ; Liu, Zheng ; Su, Wenxia

AbstractBackgroundDistant metastasis occurs in the majority of adrenocortical carcinoma (ACC), leading to an extremely poor prognosis. However, the key genes driving ACC metastasis remain unclear.MethodsWeighted gene co‐expression network analysis (WGCNA) and functional enrichment analysis were conducted to identify ACC metastasis‐related genes. Data from RNA‐seq and microarray were analyzed to reveal correlations of the CENPM gene with cancer, metastasis, and survival in ACC. Immunohistochemistry was used to assess CENPM protein expression. The impact of CENPM on metastasis behaviour was verified in ACC (H295R and SW‐13) cells and xenograft NPG mice. DIA quantitative proteomics analysis, western blot, immunofluorescence, and co‐immunoprecipitation assay were performed to identify the downstream target of CENPM.ResultsAmong the 12 035 analyzed genes, 363 genes were related to ACC metastasis and CENPM was identified as the hub gene. CENPM was upregulated in ACC samples and associated with metastasis and poor prognosis. Knockdown of CENPM inhibited proliferation, invasion, and migration of ACC cells and suppressed liver metastasis in xenograft NPG mice. Collagen‐containing extracellular matrix signalling was primarily downregulated when CENPM was knocked down. FGL1, important components of ECM signalling and immune checkpoint ligand of LAG3, were downregulated following CENPM silence, overexpressed in human advanced ACC samples, and colocalized with CENPM. Physical interaction between CENPM and FGL1 was identified. Overexpression of FGL1 rescued migration and invasion of CENPM knockdown ACC cells.ConclusionsCENPM is a key gene in driving ACC metastasis. CENPM promotes ACC metastasis through physical interaction with the immune checkpoint ligand FGL1. CENPM can be used as a new prognostic biomarker and therapeutic target for metastatic ACC.Highlights

CENPM is the key gene that drives ACC metastasis, and a robust biomarker for ACC prognosis.

Silencing CENPM impedes ACC metastasis in vitro and in vivo by physical interaction with immune checkpoint ligand FGL1.

FGL1 is overexpressed in ACC and promotes ACC metastasis.

15 Nov 2024·Journal of Clinical Investigation

TSC/mTORC1 mediates mTORC2/AKT1 signaling in c-MYC–induced murine hepatocarcinogenesis via centromere protein M

Article

Author: Lin, Shumei ; Xu, Hongwei ; Chun, Joanne ; Calvisi, Diego F. ; Song, Xinhua ; Zhang, Shu ; Cui, Guofei ; Wang, Haichuan ; Xu, Meng ; Wang, Jingwen ; Deng, Shanshan ; Chen, Nianyong ; Wang, Xue ; Yonemura, Andrew ; Deng, Youping ; Evert, Matthias ; Chen, Xin ; Zhou, Yi ; Calvisi, Diego F ; Qiu, Guoteng ; Qiu, guoteng ; Xu, Zijing

Activated mTORC2/AKT signaling plays a role in hepatocellular carcinoma (HCC). Research has shown that TSC/mTORC1 and FOXO1 are distinct downstream effectors of AKT signaling in liver regeneration and metabolism. However, the mechanisms by which these pathways mediate mTORC2/AKT activation in HCC are not yet fully understood. Amplification and activation of c-MYC are key molecular events in HCC. In this study, we explored the roles of tuberous sclerosis complex/mTORC1 (TSC/mTORC1) and FOXO1 as downstream effectors of mTORC2/AKT1 in c-MYC-induced hepatocarcinogenesis. Using various genetic approaches in mice, we found that manipulating the FOXO pathway had a minimal effect on c-MYC-induced HCC. In contrast, loss of mTORC2 inhibited c-MYC-induced HCC, an effect that was completely reversed by ablation of TSC2, which activated mTORC1. Additionally, we discovered that p70/RPS6 and 4EBP1/eIF4E acted downstream of mTORC1, regulating distinct molecular pathways. Notably, the 4EBP1/eIF4E cascade is crucial for cell proliferation and glycolysis in c-MYC-induced HCC. We also identified centromere protein M (CENPM) as a downstream target of the TSC2/mTORC1 pathway in c-MYC-driven hepatocarcinogenesis, and its ablation entirely inhibited c-MYC-dependent HCC formation. Our findings demonstrate that the TSC/mTORC1/CENPM pathway, rather than the FOXO cascade, is the primary signaling pathway regulating c-MYC-driven hepatocarcinogenesis. Targeting CENPM holds therapeutic potential for treating c-MYC-driven HCC.

01 Jul 2024·FEBS Open Bio

Exploring the role of CD8⁺ T cells in clear renal cell carcinoma metastasis

Article

Author: Meng, Lingzhang ; Ling, Caixia ; Luo, Yanhong ; Shen, Jiajia ; Qin, Yujuan ; Liang, Zhengfang ; Huang, Shaoang ; Chen, Yuanhong ; Lin, Wenxian

Clear cell renal cell carcinoma (ccRCC) accounts for approximately 75–80% of all patients with renal cell carcinoma. Despite its prevalence, little is known regarding the key components involved in ccRCC metastasis. In this study, scRNA‐seq analysis was employed to classify CD8+ T cells into four sub‐clusters based on their genetic profiles and immunofluorescence experiments were used to validate two key clusters. Through gene set enrichment analysis, these newly identified sub‐clusters were found to exhibit distinct biological characteristics. Notably, TYMP, TOP2A, CHI3L2, CDKN3, CENPM, and RZH2 were highly expressed in these sub‐clusters, indicating a correlation with poor prognosis. Among these sub‐clusters, CD8+ T cells (MT‐ND4) were identified as potentially playing a critical role in mediating ccRCC metastasis. These results contribute to our understanding of CD8+ T cell heterogeneity in ccRCC and shed light on the mechanisms underlying the loss of immune response against cancer.

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CENPM

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