Inhibition of apoptosis through AKT-mTOR pathway in ovarian cancer and renal cancer

Chen, Hongrun; Zhang, Lianfeng; Zuo, Meini; Lou, Xiaowen; Liu, Bin; Fu, Taozhu

doi:10.18632/aging.204564

Cited by 4 publications

(4 citation statements)

References 38 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In lung adenocarcinoma, upregulated STXBP1 expression correlates with poor prognosis [76]. Threonine and tyrosine kinase (TTK), alternatively referred to as unipolar spindle 1 (Mps1), acts as a spindle assembly checkpoint, guaranteeing the precise segregation of chromosomes into daughter cells [77]. Apart from the testes and placenta, TTK is rarely detected in normal tissues [78].…”

Section: Discussionmentioning

confidence: 99%

Construction of breast cancer-related gene prognostic signature in endometrial cancer

Xu,

Zhang,

Qin

et al. 2024

Preprint

View full text Add to dashboard Cite

Objective Breast cancer (BC) and endometrial cancer (EC) both originate from sex hormone-dependent organs, yet their interaction mechanisms remain unclear. This study aims to explore the common genetic and molecular characteristics between BC and EC, predicting their potential roles in EC treatment and prognosis evaluation. Methods Data on BC and EC were retrieved from The Cancer Genome Atlas Program (TCGA) and the International Cancer Genome Consortium (ICGC) databases. Differential expression analysis and weighted gene co-expression network analysis (WGCNA) were conducted to identify shared genes. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed on the shared genes. Single-factor Cox analysis, least absolute shrinkage and selection operator (LASSO) regression, and multivariate Cox regression were employed to identify potential breast cancer-related genes (BCRGs), and a prognostic risk scoring system was developed. Additionally, we examined the relationship between risk groups and clinicopathological features, immune infiltration, tumor mutation burden, and drug sensitivity. Results A total of 367 breast cancer-related DEGs were identified in EC, and 113 potentially prognostic DEGs were screened. From these, 11 key BCRGs significantly associated with the overall survival rate of EC patients were identified. Patients in the low-risk group exhibited longer overall survival (OS) compared to those in the high-risk group. Additionally, significant differences in clinical characteristics, tumor immune cell infiltration, somatic mutations, and drug sensitivity were observed between risk groups, with the low-risk group showing a higher likelihood of benefiting from immunotherapy. Conclusion The risk score established in this study demonstrates prognostic ability, potentially aiding in identifying patients who may benefit from immunotherapy and targeted therapy after breast cancer diagnosis.

show abstract

Section: Discussionmentioning

confidence: 99%

Construction of breast cancer-related gene prognostic signature in endometrial cancer

Xu,

Zhang,

Qin

et al. 2024

Preprint

View full text Add to dashboard Cite

show abstract

“…In our study, we first reported that ANXA2 interacts with TTK and acts as a molecule upstream of TTK, regulating ESCC cell growth and metastasis. Chen et al reported that TTK inhibits apoptosis through the Akt/mTOR pathway in ovarian cancer [ 49 ]. Besides, TTK was found to regulate tumor proliferation in gastric cancer, colon cancer and HCC [ 50 – 52 ].…”

Section: Discussionmentioning

confidence: 99%

Annexin A2 combined with TTK accelerates esophageal cancer progression via the Akt/mTOR signaling pathway

Liu,

Lu,

et al. 2024

Cell Death Dis

View full text Add to dashboard Cite

Annexin A2 (ANXA2) is a widely reported oncogene. However, the mechanism of ANXA2 in esophageal cancer is not fully understood. In this study, we provided evidence that ANXA2 promotes the progression of esophageal squamous cell carcinoma (ESCC) through the downstream target threonine tyrosine kinase (TTK). These results are consistent with the up-regulation of ANXA2 and TTK in ESCC. In vitro experiments by knockdown and overexpression of ANXA2 revealed that ANXA2 promotes the progression of ESCC by enhancing cancer cell proliferation, migration, and invasion. Subsequently, animal models also confirmed the role of ANXA2 in promoting the proliferation and metastasis of ESCC. Mechanistically, the ANXA2/TTK complex activates the Akt/mTOR signaling pathway and accelerates epithelial-mesenchymal transition (EMT), thereby promoting the invasion and metastasis of ESCC. Furthermore, we identified that TTK overexpression can reverse the inhibition of ESCC invasion after ANXA2 knockdown. Overall, these data indicate that the combination of ANXA2 and TTK regulates the activation of the Akt/mTOR pathway and accelerates the progression of ESCC. Therefore, the ANXA2/TTK/Akt/mTOR axis is a potential therapeutic target for ESCC.

show abstract

“…Activation of AKT is the most common signaling mechanism involved in OC cell survival, growth, and proliferation [10][11][12]. Previous studies have demonstrated that FBXL18 promotes glioblas- toma cell proliferation via promoting K63-linked ubiquitination to activate AKT signaling in human glioma cancer [13].…”

Section: Fbxl18 Is Required For Oc Cell Proliferation and Migration V...mentioning

confidence: 99%

FBXL18 is required for ovarian cancer cell proliferation and migration through activating AKT signaling

Zhuang

2024

Am J Transl Res

View full text Add to dashboard Cite

Background: F-box and leucine-rich repeat protein 18 (FBXL18) is an F-box protein that functions as an E3-ubiquitin ligase, and it plays pivotal roles in multiple disease processes. However, its role and underlying mechanism in ovarian cancer (OC) are still unknown. We investigated the impact and mechanism of FBXL18 in OC cell growth and tumorigenesis. Methods: Silent interfering RNAs and overexpression plasmids were employed to knock down and overexpress FBXL18 in OC cells (A2780 and OVCAR3). CCK-8, colony formation, cell migration, and nude mouse xenograft assays were used to assess the effect of FBXL18 on OC cell proliferation and migration. Western blotting and co-immunoprecipitation followed by ubiquitination assays were performed to detect the mechanism of the FBXL18/AKT axis in OC. Results: FBXL18 knockdown inhibited OC cell proliferation and migration, whereas FBXL18 overexpression showed the opposite results. Phosphorylated-AKT (S473) protein expression was increased by FBXL18 overexpression and markedly decreased after phosphorylated-AKT inhibitor (MK-2206) treatment. Coimmunoprecipitation assays demonstrated that FBXL18 strongly interacted with AKT in OC cells. Ubiquitination assays revealed that FBXL18 promoted K63-linked AKT ubiquitination to activate AKT. MK-2206 treatment reversed the increase in proliferation and migration of OC cells induced by FBXL18 overexpression. Conclusions: FBXL18 promoted OC cell proliferation and migration and facilitated OC tumorigenesis. Mechanically, FBXL18 interacted with AKT and promoted K63-linked ubiquitination of AKT to activate AKT in OC cells. Our study revealed that the FBXL18/AKT axis plays a crucial role in the OC process, indicating that FBXL18 may be a valuable target for OC diagnosis and treatment.

show abstract

Inhibition of apoptosis through AKT-mTOR pathway in ovarian cancer and renal cancer

Cited by 4 publications

References 38 publications

Construction of breast cancer-related gene prognostic signature in endometrial cancer

Construction of breast cancer-related gene prognostic signature in endometrial cancer

Annexin A2 combined with TTK accelerates esophageal cancer progression via the Akt/mTOR signaling pathway

FBXL18 is required for ovarian cancer cell proliferation and migration through activating AKT signaling

Contact Info

Product

Resources

About