Novel 1,3,5‐triazine derivatives exert potent anti‐cervical cancer effects by modulating Bax, Bcl2 and Caspases expression

Wang, Xiwen; Yi, Yuexiong; Lv, Qiongying; Zhang, Juan; Wu, Kejia; Wu, Wanrong; Zhang, Wei

doi:10.1111/cbdd.13133

Cited by 12 publications

(9 citation statements)

References 39 publications

(43 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Bcl-2) or induce (e.g. Bax and caspases) cell death (26). Therefore, the present study detected the protein expression levels of Bcl-2, Bax, caspase-3 and caspase-9.…”

Section: Mir-589-5p Inhibits Viability and Induces Apoptosis Of Prostate Cancer Cellsmentioning

confidence: 81%

miR‑589‑5p is downregulated in prostate cancer and regulates tumor cell viability and metastasis by targeting CCL‑5

Jiang

Mao

et al. 2019

Mol Med Report

View full text Add to dashboard Cite

Prostate cancer is one of the most common human malignancies, which represents a serious threat to health, and micrornas (mirnas/mirs) have been reported to be closely associated with the progression and development of prostate cancer. The present study aimed to investigate the expression patterns, functions and underlying mechanisms of mir-589-5p in prostate cancer. The results demonstrated that the expression levels of mir-589-5p were downregulated in prostate cancer tissues and cell lines. overexpression of mir-589-5p inhibited cell viability, migration and invasion in prostate cancer cells. Subsequently, chemokine (c-c motif) ligand 5 (CCL-5) was identified as a direct target gene of miR-589-5p, which was highly expressed at the mrna and protein levels in prostate cancer tissues and cells. Furthermore, ccl-5 mrna was negatively correlated with mir-589-5p expression in prostate cancer tissues. Silencing ccl-5 promoted the apoptosis, and inhibited the migration and invasion of prostate cancer cells. Taken together, these results indicated that mir-589-5p may act as a tumor suppressor in prostate cancer by targeting ccl-5, thus suggesting that mir-589-5p may be a novel and reliable molecular marker for the diagnosis and prognosis of prostate cancer.

show abstract

“…Bcl-2) or induce (e.g. Bax and caspases) cell death (26). Therefore, the present study detected the protein expression levels of Bcl-2, Bax, caspase-3 and caspase-9.…”

Section: Mir-589-5p Inhibits Viability and Induces Apoptosis Of Prostate Cancer Cellsmentioning

confidence: 81%

miR‑589‑5p is downregulated in prostate cancer and regulates tumor cell viability and metastasis by targeting CCL‑5

Jiang

Mao

et al. 2019

Mol Med Report

View full text Add to dashboard Cite

show abstract

“…Regarding the mechanism, Bcl-2 mRNA has been demonstrated to be a direct target of miR-744 in cervical cancer [31]. Bcl-2, an integral protein of the outer mitochondrial membrane, is strongly implicated in the initiation and malignant progression of cervical cancer by regulating cell proliferation, viability, cell cycle progression, apoptosis, epithelial-mesenchymal transition, migration, invasion, and metastasis [39][40][41]. Bcl-2 is reported as a double-edged sword by inducing apoptosis and inhibiting apoptosis at the same time [42,43].…”

Section: Discussionmentioning

confidence: 99%

Long noncoding RNA RUSC1-AS1 promotes tumorigenesis in cervical cancer by acting as a competing endogenous RNA of microRNA-744 and consequently increasing Bcl-2 expression

Guo

Zhang

et al. 2020

Cell Cycle

View full text Add to dashboard Cite

The expression of a long noncoding RNA termed RUSC1-AS1 is dysregulated in breast cancer and laryngeal squamous cell carcinoma, and this dysregulation affects various tumor-associated biological processes. To our knowledge, the expression status and detailed roles of RUSC1-AS1 in cervical cancer as well as its regulatory mechanisms of action remain unknown. Therefore, the objectives of this study were to measure RUSC1-AS1 expression in cervical cancer, investigate the effects of RUSC1-AS1 on cervical cancer cells, and identify the mechanism underlying these effects. Herein, RUSC1-AS1 was found to be highly expressed in cervical cancer tissues and cell lines. High RUSC1-AS1 expression significantly correlated with the International Federation of Gynecology and Obstetrics (FIGO) stage, lymph node metastasis, and shorter overall survival among the patients with cervical cancer. Functional assays revealed that interference with RUSC1-AS1 expression suppressed cervical cancer cell proliferation, migration, and invasion in vitro; induced apoptosis in vitro; and impeded tumor growth in vivo. In addition, RUSC1-AS1 was demonstrated to act as a competing endogenous RNA of microRNA-744 (miR-744) and consequently increase B-cell lymphoma 2 (Bcl-2 or BCL2) expression levels in cervical cancer cells. Furthermore, either inhibition of miR-744 or restoration of Bcl-2 expression neutralized the effects of the RUSC1-AS1 silencing on the malignant characteristics of cervical cancer cells. Thus, RUSC1-AS1 promotes the aggressiveness of cervical cancer in vitro and in vivo by upregulating miR-744-Bcl-2 axis output. The RUSC1-AS1-miR-744-Bcl-2 pathway may be involved in cervical cancer pathogenesis and could serve as a novel target for anticancer therapies.

show abstract

“…Studies have shown that inhibitors of the autophagy gene ATG4 can inhibit autophagy, enhance the cytotoxicity of chemotherapy drugs, and achieve the purpose of killing tumor cells [ 29 ]. Autophagy gene BCL2 can be used as a therapeutic target of some drugs for cervical cancer [ 30 ]. TM9SF1 can bind to the estrogen receptors, regulate the epithelial-mesenchymal transformation of cancer cells, and promote tumor metastasis [ 31 ].…”

Section: Discussionmentioning

confidence: 99%

Identification and Validation of Autophagy-Related Gene Nomograms to Predict the Prognostic Value of Patients with Cervical Cancer

Jiang

Wang

et al. 2021

Journal of Oncology

View full text Add to dashboard Cite

Autophagy is a process of engulfing one’s own cytoplasmic proteins or organelles and coating them into vesicles, fusing with lysosomes to form autophagic lysosomes, and degrading the contents it encapsulates. Increasing studies have shown that autophagy disorders are closely related to the occurrence of tumors. However, the prognostic role of autophagy genes in cervical cancer is still unclear. In this study, we constructed risk signatures of autophagy-related genes (ARGs) to predict the prognosis of cervical cancer. The expression profiles and clinical information of autophagy gene sets were downloaded from TCGA and GSE52903 queues as training and validation sets. The normal cervical tissue expression profile data from the UCSC XENA website (obtained from GTEx) were used as a supplement to the TCGA normal cervical tissue. Univariate COX regression analysis of 17 different autophagy genes was performed with the consensus approach. Tumor samples from TCGA were divided into six subtypes, and the clinical traits of the six subtypes had different distributions. Further absolute shrinkage and selection operator (LASSO) and multivariable COX regression yielded an autophagy genetic risk model consisting of eight genes. In the training set, the survival rate of the high-risk group was lower than that of the low-risk group ( p < 0.0001). In the validation set, the AUC area of the receiver operating characteristic (ROC) curve was 0.772 for the training set and 0.889 for the verification set. We found that high and low risk scores were closely related to TNM stage ( p < 0.05). The nomogram shows that the risk score combined with other indicators, such as G, T, M, and N, better predicts 1-, 3-, and 5-year survival rates. Decline curve analysis (DCA) shows that the risk model combined with other indicators produces better clinical efficacy. Immune cells with an enrichment score of 28 showed statistically significant differences related to high and low risk. GSEA enrichment analysis showed the main enrichment being in KRAS activation, genes defining epithelial and mesenchymal transition (EMT), raised in response to the low oxygen level (hypoxia) gene and NF-kB in response to TNF. These pathways are closely related to the occurrence of tumors. Our constructed autophagy risk signature may be a prognostic tool for cervical cancer.

show abstract

Novel 1,3,5‐triazine derivatives exert potent anti‐cervical cancer effects by modulating Bax, Bcl2 and Caspases expression

Cited by 12 publications

References 39 publications

miR‑589‑5p is downregulated in prostate cancer and regulates tumor cell viability and metastasis by targeting CCL‑5

miR‑589‑5p is downregulated in prostate cancer and regulates tumor cell viability and metastasis by targeting CCL‑5

Long noncoding RNA RUSC1-AS1 promotes tumorigenesis in cervical cancer by acting as a competing endogenous RNA of microRNA-744 and consequently increasing Bcl-2 expression

Identification and Validation of Autophagy-Related Gene Nomograms to Predict the Prognostic Value of Patients with Cervical Cancer

Contact Info

Product

Resources

About