Paclitaxel Promotes Cell Apoptosis in Uterine Leiomyomas

Li, Haiping; Wang, Qianqian; Sheng, Lianbing; Zhang, Yan; Li, Yunfei; Hao, Tianyu

doi:10.1159/000479161

Cited by 7 publications

(4 citation statements)

References 26 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The antitumor effects of PTX have been attributed to defects in mitotic spindle assembly, chromosome segregation, and cell division. Previous studies have found that PTX can induce apoptosis in different cancer cell lines . However, recent studies have found that PTX can also inhibit EMT related proteins, similar to Zn .…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Zinc promotes prostate cancer cell chemosensitivity to paclitaxel by inhibiting epithelial‐mesenchymal transition and inducing apoptosis

Xue

Liu

et al. 2019

The Prostate

View full text Add to dashboard Cite

Background: Paclitaxel (PTX) is a first-line chemotherapeutic drug for the treatment of prostate cancer. However, most patients develop resistance and metastasis, and thus new therapeutic approaches are urgently required. Recent studies have identified widespread anti-tumor effects of zinc (Zn) in various tumor cell lines, especially prostate cancer cells. In this study, we examined the effects of Zn as an adjuvant to PTX in prostate cancer cells. Methods: PC3 and DU145 cells were treated with different concentrations of Zn and/ or PTX. MTT assay was used to detect cell viability. Real-time cell analysis (RTCA) and microscopy were used to observe morphological changes in cells. Western blotting was used to detect the expression of epithelial-mesenchymal transition (EMT)-related proteins. qPCR (reverse transcription-polymerase chain reaction) was used to examine changes in TWIST1 mRNA levels. Cell invasion and migration were detected by scratch and transwell assays. shRNA against TWIST1 was used to knockdown TWIST1. Colony formation assay was used to detect cell proliferation, while Annexin V and propidium iodide (PI) staining was used to detect cell apoptosis. Results: Zn and PTX increased proliferation inhibition in a dose-and time-dependent manner in prostate cancer cells, while Zn increased prostate cancer cell chemosensitivity to PTX. Combined Zn and PTX inhibited prostate cancer cell invasion and migration by downregulating the expression of TWIST1. Furthermore, knockdown of TWIST1 increased the sensitivity of prostate cancer cells to PTX. In addition, Zn and PTX reduced cell proliferation and induced apoptosis in prostate cancer cells.Conclusions: Our results demonstrated that Zn and PTX combined therapy inhibits EMT by reducing the expression of TWIST1, which reduces the invasion and migration of prostate cancer cells. SiTWIST1 increased the sensitivity of prostate cancer cells to PTX. In addition, with prolonged treatment, Zn and PTX inhibited proliferation and led to prostate cancer cell apoptosis. Therefore, Zn may be a potential adjuvant of PTX in treating prostate cancer and combined treatment may offer a promising therapeutic strategy for prostate cancer. K E Y W O R D S

show abstract

Section: Introductionmentioning

confidence: 99%

“…Previous studies have found that PTX can induce apoptosis in different cancer cell lines. [22][23][24] However, recent studies have found that PTX can also inhibit EMT related proteins, similar to Zn. 25,26 Therefore, the combination of Zn and PTX may contribute to the prevention of prostate cancer resistance and metastasis.…”

Section: Introductionmentioning

confidence: 99%

Zinc promotes prostate cancer cell chemosensitivity to paclitaxel by inhibiting epithelial‐mesenchymal transition and inducing apoptosis

Xue

Liu

et al. 2019

The Prostate

View full text Add to dashboard Cite

show abstract

“…Paclitaxel accelerates the formation of microtubules from microtubule dimers and prevents their separation, which induces abnormal mechanical reorganization of the microtubules and inhibits normal cell division. This drug also inhibits the effects of other factors on the microtubule system and, together with the stable binding of microtubule proteins, eventually induces apoptosis ( Liu et al, 2017a ). In clinical applications, paclitaxel has shown good efficacy in treating non-small cell lung cancer ( Hoang et al, 2012 ), breast cancer ( Manhas et al, 2022 ), gastric cancer ( Tu et al, 2022 ), nasopharyngeal cancer ( Xia et al, 2022 ), ovarian cancer ( Kong et al, 2023 )and cervical cancer ( Yasunaga et al, 2022 ), particularly for drug-resistant tumors ( Song et al, 2018 ; Kawiak et al, 2019 ).…”

Section: Introductionmentioning

confidence: 99%

Mechanism of action of paclitaxel for treating glioblastoma based on single-cell RNA sequencing data and network pharmacology

Rao

et al. 2022

Front. Pharmacol.

View full text Add to dashboard Cite

Paclitaxel is an herbal active ingredient used in clinical practice that shows anti-tumor effects. However, its biological activity, mechanism, and cancer cell-killing effects remain unknown. Information on the chemical gene interactions of paclitaxel was obtained from the Comparative Toxicogenomics Database, SwishTargetPrediction, Binding DB, and TargetNet databases. Gene expression data were obtained from the GSE4290 dataset. Differential gene analysis, Kyoto Encyclopedia of Genes and Genomes, and Gene Ontology analyses were performed. Gene set enrichment analysis was performed to evaluate disease pathway activation; weighted gene co-expression network analysis with diff analysis was used to identify disease-associated genes, analyze differential genes, and identify drug targets via protein-protein interactions. The Molecular Complex Detection (MCODE) analysis of critical subgroup networks was conducted to identify essential genes affected by paclitaxel, assess crucial cluster gene expression differences in glioma versus standard samples, and perform receiver operator characteristic mapping. To evaluate the pharmacological targets and signaling pathways of paclitaxel in glioblastoma, the single-cell GSE148196 dataset was acquired from the Gene Expression Omnibus database and preprocessed using Seurat software. Based on the single-cell RNA-sequencing dataset, 24 cell clusters were identified, along with marker genes for the two different cell types in each cluster. Correlation analysis revealed that the mechanism of paclitaxel treatment involves effects on neurons. Paclitaxel may affect glioblastoma by improving glucose metabolism and processes involved in modulating immune function in the body.

show abstract

“…Paclitaxel is used as a first-line treatment for advanced diseases (breast, ovarian, and lung cancers), as monotherapy or combination therapy (3). Numerous phase I and phase II trials have been reported, suggesting the potential effect of paclitaxel in treating advanced gastric cancers (4,5). It inhibits microtubule depolymerization, causes cell cycle arrest at the G 2 /M phase and suppresses tumor growth (6).…”

mentioning

confidence: 99%

Fluoxetine Enhances Anti-tumor Activity of Paclitaxel in Gastric Adenocarcinoma Cells by Triggering Apoptosis and Necroptosis

Khing

Sohn

2019

Anticancer Res

View full text Add to dashboard Cite

Background/Aim: Fluoxetine, an antidepressant, has cytotoxic effects on several cancer cell lines, while paclitaxel is an antineoplastic agent for various cancers. The aim of this study was to evaluate whether fluoxetine enhances the cytotoxic effect of paclitaxel in gastric adenocarcinoma cells and determine the mechanism of cell death. Materials and Methods: 3-( 4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay was used to examine cell viability and perform cell cycle analysis. Annexin V propidium iodide (PI) staining, 4',6-diamidino-2-phenylindole (DAPI) staining, caspase-3/7 assay, and western blot analysis were performed for determining cell death. Results: Fluoxetine enhanced the anti-proliferative effect of paclitaxel. Fluoxetine-paclitaxel combination caused G 2 /M arrest and increased events in the sub G 0 /G 1 phase in a time and dose-dependent manner, indicating apoptotic cell death. Combination treatment caused an increase in early apoptotic and late apoptotic cell death compared to single treatment alone. Conclusion: Fluoxetine enhanced the antiproliferation effect of paclitaxel in gastric adenocarcinoma AGS cells and the combination caused cell death by triggering apoptosis and necroptosis.

show abstract

Paclitaxel Promotes Cell Apoptosis in Uterine Leiomyomas

Cited by 7 publications

References 26 publications

Zinc promotes prostate cancer cell chemosensitivity to paclitaxel by inhibiting epithelial‐mesenchymal transition and inducing apoptosis

Zinc promotes prostate cancer cell chemosensitivity to paclitaxel by inhibiting epithelial‐mesenchymal transition and inducing apoptosis

Mechanism of action of paclitaxel for treating glioblastoma based on single-cell RNA sequencing data and network pharmacology

Fluoxetine Enhances Anti-tumor Activity of Paclitaxel in Gastric Adenocarcinoma Cells by Triggering Apoptosis and Necroptosis

Contact Info

Product

Resources

About