Targeting USP10 induces degradation of oncogenic ANLN in esophageal squamous cell carcinoma

Cao, Yufei; Xie, Lei; Tong, Bei-Bei; Chu, Man-Yu; Shi, Wei; Li, Xiang; He, Jianzhong; Wang, Shaohong; Wu, Zhi‐Yong; Deng, Dan-Xia; Zheng, Ya-Qi; Li, Zhi-Mao; Xu, Xiu‐E; Liao, Lian‐Di; Cheng, Yin-Wei; Li, Liyan; Xu, Li‐Yan; Li, En-Min

doi:10.1038/s41418-022-01104-x

Cited by 19 publications

(3 citation statements)

References 63 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…ANLN with the m6A modification has a crucial function in liver cancer bone metastasis [21,[33][34][35]. Cao et al reported that inhibiting the USP10-ANLN axis hinders the cell cycle progression of esophageal squamous cell carcinoma (ESCC) [36]. Our study revealed elevated ANLN expression levels in GBC tissues.…”

Section: Discussionsupporting

confidence: 52%

ANLN Promotes the Proliferation and Migration of Gallbladder Cancer Cells via STRA6-Mediated Activation of PI3K/AKT Signaling

Zhu,

Zhang,

Bian

et al. 2024

Cancers

View full text Add to dashboard Cite

The ANLN gene encodes anillin, a protein that binds to actin. Recent research has identified ANLN’s function in the initiation and advancement of different cancers. However, its impact on gallbladder cancer (GBC) remains unexplored. This study aimed to elucidate its possible molecular mechanisms in GBC. ANLN expression was assessed using quantitative real-time polymerase chain reaction (QRT-PCR), Western blotting (WB), and immunohistochemistry (IHC), revealing elevated levels in GBC tissues. ANLN knockdown resulted in the inhibition of cell proliferation and migration, leading to apoptosis and cell cycle arrest. Conversely, ANLN overexpression had the opposite effects on GBC cells. In vivo experiments confirmed that ANLN knockdown inhibited GBC cell growth. RNA-seq and bioinformatics analysis revealed ANLN’s function in activating the PI3K/AKT signaling pathway. We further confirmed that ANLN could upregulate STRA6 expression, which activated PI3K/AKT signaling to enhance the growth and movement of GBC cells. These findings demonstrate ANLN’s involvement in GBC initiation and progression, suggesting its potential as a novel target for GBC.

show abstract

Section: Discussionsupporting

confidence: 52%

ANLN Promotes the Proliferation and Migration of Gallbladder Cancer Cells via STRA6-Mediated Activation of PI3K/AKT Signaling

Zhu,

Zhang,

Bian

et al. 2024

Cancers

View full text Add to dashboard Cite

show abstract

“…2D ). Previous studies have reported that deubiquitinases (DUBs) could stabilize the protein expression by deubiquitinating the targeting proteins [ 26 , 27 ], we thus further explore whether USP10 affects the protein expression of AMTIN. It was found that overexpressing USP10 increased the protein expression of ATMIN, while silencing USP10 exerted the opposite effect (Fig.…”

Section: Resultsmentioning

confidence: 99%

Transcription factor ATMIN facilitates chemoresistance in nasopharyngeal carcinoma

Fang,

Li,

Lin

et al. 2024

Cell Death Dis

View full text Add to dashboard Cite

Despite that the docectaxel-cisplatin-5-fluorouracil (TPF) induction chemotherapy has greatly improved patients’ survival and became the first-line treatment for advanced nasopharyngeal carcinoma (NPC), not all patients could benefit from this therapy. The mechanism underlying the TPF chemoresistance remains unclear. Here, by analyzing gene-expression microarray data and survival of patients who received TPF chemotherapy, we identify transcription factor ATMIN as a chemoresistance gene in response to TPF chemotherapy in NPC. Mass spectrometry and Co-IP assays reveal that USP10 deubiquitinates and stabilizes ATMIN protein, resulting the high-ATMIN expression in NPC. Knockdown of ATMIN suppresses the cell proliferation and facilitates the docetaxel-sensitivity of NPC cells both in vitro and in vivo, while overexpression of ATMIN exerts the opposite effect. Mechanistically, ChIP-seq combined with RNA-seq analysis suggests that ATMIN is associated with the cell death signaling and identifies ten candidate target genes of ATMIN. We further confirm that ATMIN transcriptionally activates the downstream target gene LCK and stabilizes it to facilitate cell proliferation and docetaxel resistance. Taken together, our findings broaden the insight into the molecular mechanism of chemoresistance in NPC, and the USP10-ATMIN-LCK axis provides potential therapeutic targets for the management of NPC.

show abstract

“…ANLN enhances the metastasis of lung adenocarcinoma by promoting epithelial-mesenchymal transformation [16]. Targeting USP10-ANLN axis can effectively inhibit the progression of cell cycle in ESCC [17]. Overall, the high expression of ANLN leads to abnormal cell division, thereby promoting the proliferation, migration, and invasion of cancer cells [18][19][20][21][22][23].…”

Section: Introductionmentioning

confidence: 99%

Network Analysis of Differential Expression of ANLN and Its Interacting Proteins in Esophageal Squamous Cell Carcinoma

Sun,

Cao,

et al. 2023

austinjbiosensbioelectron

View full text Add to dashboard Cite

Anillin (ANLN) is an actin binding protein, which was originally extracted from Drosophila melanogaster embryos. As a key regulatory factor in cytokinesis, ANLN is highly expressed in various tumors, leading to abnormal cell division and promoting the proliferation, migration, and invasion of cancer cells. At present, the role and regulatory mechanism of ANLN in human Esophageal Squamous Cell Carcinoma (ESCC) are not fully understood. The purpose of this study is to construct a Protein-Protein Interaction Network (PPIN) to reveal the characteristics of ANLN and its interacting proteins, by the integration of their expression in ESCC. The differentially expressed ANLN and its interacting proteins in ESCC were identified from our previous RNA-seq data. By constructing a specific PPI network, it was found that many differentially expressed genes/proteins may interact with ANLN. Multiple enrichment pathways of ANLN and its differentially expressed genes were explained by functional enrichment analysis, Gene Ontology (GO) analysis and KEGG pathway analysis. In addition, it is revealed that ANLN, ECT2, ACADM and PPP1R9A play an important role in the occurrence and development of ESCC, and they are proposed as new prognostic factors for ESCC. These bioinformatics analyses provide a comprehensive perspective for the role of ANLN in ESCC.

show abstract

Targeting USP10 induces degradation of oncogenic ANLN in esophageal squamous cell carcinoma

Cited by 19 publications

References 63 publications

ANLN Promotes the Proliferation and Migration of Gallbladder Cancer Cells via STRA6-Mediated Activation of PI3K/AKT Signaling

ANLN Promotes the Proliferation and Migration of Gallbladder Cancer Cells via STRA6-Mediated Activation of PI3K/AKT Signaling

Transcription factor ATMIN facilitates chemoresistance in nasopharyngeal carcinoma

Network Analysis of Differential Expression of ANLN and Its Interacting Proteins in Esophageal Squamous Cell Carcinoma

Contact Info

Product

Resources

About