Natural Terpenoids Against Female Breast Cancer: A 5-year Recent Research

Ateba, Sylvin Benjamin; Mvondo, Marie Alfrede; Ngeu, Sadrine Tchoukouegno; Tchoumtchoua, Job; Awounfack, Charline Florence; Njamen, Dieudonné; Krenn, Liselotte

doi:10.2174/0929867325666180214110932

Cited by 56 publications

(30 citation statements)

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“…Celastrol, derived from the Chinese herbal medicine Trypterygium, exhibits extensive biological and pharmacological activities. Zhang J claimed that celastrol ameliortes inflammation on Human Retinal Pigment Epithelial Cells .…”

Section: Introductionmentioning

confidence: 99%

Antitumor activity of celastrol by inhibition of proliferation, invasion, and migration in cholangiocarcinoma via PTEN/PI3K/Akt pathway

Zhu

Wei

2019

Cancer Medicine

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Aim: Cholangiocarcinoma is a malignant tumor originating from bile duct epithelium. Currently, the treatment strategy is very limited and the prognosis is poor.Recent studies reported celastrol exhibits antigrowth and antimetastasis properties in many tumors. Our study aimed to assess the anti-CCA effects of cholangiocarcinoma (CCA) and the mechanisms involved in it. Methods: In this study, the long-term and short-term antiproliferation effects was determined using colony formation and Cell Counting Kit-8 (CCK-8) assays, respectively. Flow cytometry was performed to quantify apoptosis. Furthermore, wound healing and transwell assays were performed to determine the cell migration and invasion capabilities, respectively. To further find the mechanism involved in the celastrol-induced biological functions, LY204002, a PI3K/Akt signaling inhibitor, and an Akt-1 overexpression plasmid were employed to find whether PI3K/Akt pathway was involved in the celastrol-induced CCA cell inhibition. Additionally, short interfering RNA (siRNA) was also used to investigate the mechanism involved in the celastrol-induced PI3K/Akt signaling inhibition. Western blotting and immunofluorescence assays were also performed to detect the degree of relative proteins.Moreover, we validated the antiproliferation and antimetastasis effects of celastrol in vivo by constructing subcutaneous and lung metastasis nude mice models. Results: We discovered that celastrol effectively induced apoptotic cell death and inhibited the capacity of migration and invasion in CCA cells. Further mechanistic study identified that celastrol regulated the PI3K/Akt signaling pathway, and the antitumor efficacy was likely due to the upregulation of PTEN, a negative regulator of PI3K/Akt. Blockage of PTEN abolished the celastrol-induced PI3K/Akt signaling inhibition. Additionally, in vivo experiments conformed celastrol inhibited the tumor growth and lung metastasis with no serious side effects. Conclusions: Overall, our study elucidated a mechanistic framework for the anti-CCA effects of celastrol via PTEN/PI3K/Akt pathway. 784 | ZHU and WEI K E Y W O R D S Akt, apoptosis, celastrol, epithelial-to-mesenchymal transition, phosphatase and tensin homolog

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Section: Introductionmentioning

confidence: 99%

Antitumor activity of celastrol by inhibition of proliferation, invasion, and migration in cholangiocarcinoma via PTEN/PI3K/Akt pathway

Zhu

Wei

2019

Cancer Medicine

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“…In 1970 s, triptolide was first isolated from traditional Chinese herb Tripterygium wilfordii HOOK F. and purified. 25) As the progress in pharmacological research of triptolide, it has been reported to exhibit a clinical significance in anti-cancer treatment. 26,27) Previous studies have showed that more than one signaling pathway attributing to the anti-tumor effect of triptolide.…”

Section: Discussionmentioning

confidence: 99%

Triptolide Suppresses Growth of Breast Cancer by Targeting HMGB1 <i>in Vitro</i> and <i>in Vivo</i>

Jiang

Chen

Xiao

et al. 2019

Biological & Pharmaceutical Bulletin

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Triptolide has been indicated potent anti-cancer effect involving multiple molecular targets and signaling pathways. High-mobility group box 1 (HMGB1) is a highly conserved DNA-binding protein taking part in breast cancer development. The therapeutic effect of triptolide on HMGB1 has not been reported. Thus, our study aims to clarify the role of HMGB1 in triptolide-induced anti-growth effect on breast cancer in vitro and in vivo. We demonstrated that triptolide significantly suppressed growth of breast cancer cells by inhibition of cell viability, clonogenic ability. Further studies evidenced that triptolide treatment not only inhibited HMGB1 mRNA expression, but also decreased supernatant level of HMGB1 in vitro. In line with these observations, exogenous recombinant HMGB1 (rHMGB1) promoted cell proliferation of breast cancer, and triptolide reversed the rHMGB1-promoted proliferative effect. As well, triptolide enhanced the antiproliferative activity of ethyl pyruvate (EP) (HMGB1 inhibitor). Furthermore, downstream correlation factors (Toll-like receptor 4 (TLR4) and phosphorylated-nuclear factor-kappaB (NF-κB) p65) of HMGB1 were significantly decreased in vitro after triptolide treatment. Consistantly, we confirmed that tumor growth was significantly inhibited after triptolide treatment in vivo. Meanwhile, immunohistochemical analyses showed that triptolide treatment significantly decreased the level of cytoplasmic HMGB1 and TLR4 expression, whereas the expression of NF-κB p65 was relatively higher in cytoplasm, and conversely lower in nucleus as compared to the control group. Collectively, these results demonstrate that triptolide suppresses the growth of breast cancer cells via reduction of HMGB1 expression in vitro and in vivo, which may provide new insights into the treament of breast cancer.

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“…The metastasis involves dissemination of cancer cells and is the leading cause of mortality in breast cancer patients [ 3 ]. With advances in understanding the pathogenesis of breast cancer, many natural phytochemicals have been reported to be promising for treatment of female breast cancer [ 4 ]. However, more studies are needed to better understand their pharmacology in treating TNBC.…”

Section: Introductionmentioning

confidence: 99%

Celastrol Inhibits Migration and Invasion of Triple-Negative Breast Cancer Cells by Suppressing Interleukin-6 via Downregulating Nuclear Factor-κB (NF-κB)

Yan

et al. 2020

Med Sci Monit

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Natural Terpenoids Against Female Breast Cancer: A 5-year Recent Research

Abstract: These compounds appear to be promising to overcome breast cancer treatment failure. However, despite the interesting activities, additional preclinical investigations are needed in further breast cancer cell/tumor models in vitro and in vivo.

Cited by 56 publications

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Antitumor activity of celastrol by inhibition of proliferation, invasion, and migration in cholangiocarcinoma via PTEN/PI3K/Akt pathway

Antitumor activity of celastrol by inhibition of proliferation, invasion, and migration in cholangiocarcinoma via PTEN/PI3K/Akt pathway

Triptolide Suppresses Growth of Breast Cancer by Targeting HMGB1 <i>in Vitro</i> and <i>in Vivo</i>

Celastrol Inhibits Migration and Invasion of Triple-Negative Breast Cancer Cells by Suppressing Interleukin-6 via Downregulating Nuclear Factor-κB (NF-κB)

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