Indirubin suppresses ovarian cancer cell viabilities through the STAT3 signaling pathway

Wang, Jinhua; Wu, Jianbo; Zheng, Qiaomei; Hu, Jifen

doi:10.2147/dddt.s174613

Cited by 32 publications

(22 citation statements)

References 24 publications

(31 reference statements)

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“…Indirubin has been shown to impede cyclin-dependent kinase dimers, triggering cell cycle arrest at G1/S or G2/M phase. Additionally, it repressed phosphorylated STAT3 expression [234].…”

Section: Indirubinmentioning

confidence: 99%

Targeting the JAK/STAT Signaling Pathway Using Phytocompounds for Cancer Prevention and Therapy

Bose¹,

Banerjee²,

Mondal³

et al. 2020

Cells

145

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Cancer is a prevalent cause of mortality around the world. Aberrated activation of Janus kinase (JAK)/signal transducer and activator of transcription (STAT) signaling pathway promotes tumorigenesis. Natural agents, including phytochemicals, exhibit potent anticancer activities via various mechanisms. However, the therapeutic potency of phytoconstituents as inhibitors of JAK/STAT signaling against cancer has only come into focus in recent days. The current review highlights phytochemicals that can suppress the JAK/STAT pathway in order to impede cancer cell growth. Various databases, such as PubMed, ScienceDirect, Web of Science, SpringerLink, Scopus, and Google Scholar, were searched using relevant keywords. Once the authors were in agreement regarding the suitability of a study, a full-length form of the relevant article was obtained, and the information was gathered and cited. All the complete articles that were incorporated after the literature collection rejection criteria were applied were perused in-depth and material was extracted based on the importance, relevance, and advancement of the apprehending of the JAK/STAT pathway and their relation to phytochemicals. Based on the critical and comprehensive analysis of literature presented in this review, phytochemicals from diverse plant origins exert therapeutic and cancer preventive effects, at least in part, through regulation of the JAK/STAT pathway. Nevertheless, more preclinical and clinical research is necessary to completely comprehend the capability of modulating JAK/STAT signaling to achieve efficient cancer control and treatment.

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“…Indirubin has been shown to impede cyclin-dependent kinase dimers, triggering cell cycle arrest at G1/S or G2/M phase. Additionally, it repressed phosphorylated STAT3 expression [234].…”

Section: Indirubinmentioning

confidence: 99%

Targeting the JAK/STAT Signaling Pathway Using Phytocompounds for Cancer Prevention and Therapy

Bose¹,

Banerjee²,

Mondal³

et al. 2020

Cells

145

View full text Add to dashboard Cite

show abstract

“…To further test whether lower levels of phospho-JAK2/STAT3 was the cause of lactucin-mediated anti-adipogenesis, cells were treated with colivelin, a specific activator of STAT3 [34][35][36]. First, the activation of STAT3 by colivelin was examined.…”

Section: Pharmacological Stat3 Activator Reverses the Anti-adipogenicmentioning

confidence: 99%

A Potential Nutraceutical Candidate Lactucin Inhibits Adipogenesis through Downregulation of JAK2/STAT3 Signaling Pathway-Mediated Mitotic Clonal Expansion

Wang

Liu

Cai

et al. 2020

Cells

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The prevalence of obesity has increased dramatically worldwide in the past ~50 years. Searching for safe and effective anti-obesity strategies are urgently needed. Lactucin, a plant-derived natural small molecule, is known for anti-malaria and anti-hyperalgesia. The study is to investigate whether lactucin plays a key role in adipogenesis. To this end, in vivo male C57BL/6 mice fed a high-fat diet (HFD) were treated with 20 mg/kg/day of lactucin or vehicle by gavage for seven weeks. Compared with vehicle-treated controls, Lactucin-treated mice showed lower body mass and mass of adipose tissue. Consistently, in vitro 3T3-L1 cells were treated with 20 μM of lactucin. Compared to controls, lactucin-treated cells showed significantly less lipid accumulation during adipocyte differentiation and lower levels of lipid synthesis markers. Mechanistically, we showed the anti-adipogenic property of lactucin was largely limited to the early stage of adipogenesis. Lactucin-treated cells fail to undergo mitotic clonal expansion (MCE). Further studies demonstrate that lactucin-induced MCE arrests might result from reduced phosphorylation of JAK2 and STAT3. We then asked whether activation of JAK2/STAT3 would restore the inhibitory effect of lactucin on adipogenesis with pharmacological STAT3 activator colivelin. Our results revealed similar levels of lipid accumulation between lactucin-treated cells and controls in the presence of colivelin, indicating that inactivation of STAT3 is the limiting factor for the anti-adipogenesis of lactucin in these cells. Together, our results provide the indication that lactucin exerts an anti-adipogenesis effect, which may open new therapeutic options for obesity.

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“…STAT3 enhances various signaling pathways involved in the regulation of cell growth, invasion and EMT, and is recognized as a key target for cancer treatment (40)(41)(42). The STAT3 signaling pathway plays an important role in ovarian cancer progression (43)(44)(45). In order to explore the molecular mechanism behind the role of lncRNA-ATB in ovarian cancer, the STAT3 pathway was analyzed.…”

Section: Discussionmentioning

confidence: 99%

Role of lncRNA‑ATB in ovarian cancer and its mechanisms of action

et al. 2019

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This study aimed to elucidate the role of long non-coding RNA activated by transforming growth factor-β (lncRNA-ATB) in ovarian cancer and its underlying mechanisms of action. Expression levels of lncRNA-ATB in ovarian cancer cell line SKOV3 and in a healthy human ovarian cell line were compared using reverse transcription-quantitative polymerase chain reaction (RT-qPCR). The results indicated that lncRNA-ATB was expressed at significantly higher levels in SKOV3 cells compared with the healthy cell line. After downregulation of lncRNA-ATB expression in SKOV3 cells using lncRNA-ATB-short hairpin RNA, cell proliferation, apoptosis, invasion and migration were assessed using Cell counting kit-8, Live Dead staining, Transwell assay and wound healing assay, respectively. RT-qPCR and western blotting were used to quantify the expression of signal transducer and activator of transcription 3 (STAT3), phosphorylated (p)-STAT3, and the additional epithelial to mesenchymal transition (EMT)-related proteins E-cadherin and vimentin in SKOV3 cells. LncRNA-ATB downregulation significantly reduced SKOV3 cell proliferation, invasion and migration, promoted apoptosis, decreased the expression of p-STAT3 and vimentin, and increased E-cadherin expression. Taken together, these results suggest that lncRNA-ATB downregulation can inhibit ovarian cancer cell proliferation, invasion and migration, and promote cell apoptosis. Lnc-RNA-ATB may therefore be a new target for ovarian cancer treatment.

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Indirubin suppresses ovarian cancer cell viabilities through the STAT3 signaling pathway

Cited by 32 publications

References 24 publications

Targeting the JAK/STAT Signaling Pathway Using Phytocompounds for Cancer Prevention and Therapy

Targeting the JAK/STAT Signaling Pathway Using Phytocompounds for Cancer Prevention and Therapy

A Potential Nutraceutical Candidate Lactucin Inhibits Adipogenesis through Downregulation of JAK2/STAT3 Signaling Pathway-Mediated Mitotic Clonal Expansion

Role of lncRNA‑ATB in ovarian cancer and its mechanisms of action

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