Oridonin Suppresses Proliferation of Human Ovarian Cancer Cells via Blockage of mTOR Signaling

Xiao, Rong; Chen, Sunxiao; Qin, Qin; Chen, Yan; Zhang, Weiwei; Zhu, Rongrong; Deng, An-mei

doi:10.7314/apjcp.2016.17.2.667

Cited by 18 publications

(10 citation statements)

References 19 publications

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“…Numerous studies show that oridonin can suppress cell growth and induce cell-cycle arrest in a variety of cancer cell lines (2,5,6). Oridonin also causes a reduction in cell proliferation through induction of death receptor 5 and suppression of mammalian target of rapamycin (mTOR) phosphorylation in breast and ovarian cancer cells (13,14). In the present study, we investigated whether oridonin has growth inhibitory activity in human oral cancer cells.…”

Section: Discussionmentioning

confidence: 98%

Oridonin induces apoptosis in human oral cancer cells via phosphorylation of histone H2AX

Yang

Shin

Lee

et al. 2017

European J Oral Sciences

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Oridonin, a natural diterpenoid purified from Rabdosia rubescens, has displayed beneficial biological activities, including anti-proliferation and anti-angiogenesis effects, in various types of cancers. However, the anti-cancer potential of oridonin and its mechanism in oral cancer have never previously been studied. In this study, we assessed the role of oridonin as an inducer of apoptosis in HSC-3 and HSC-4 human oral cancer cells. Our results showed that oridonin reduces the viability of human oral cancer cells and significantly increases the expression of γH2AX, a well-known marker of DNA damage. 4',6-Diamidino-2-phenylindole (DAPI) staining and western blotting showed that oridonin causes nuclear condensation and fragmentation, and induces cleavage of poly(ADP-ribose) polymerase (PARP). Moreover, oridonin-induced γH2AX accumulation was partially abrogated by Z-VAD, a pan-caspase inhibitor. Taken together, our results suggest that oridonin can effectively induce apoptosis by augmenting the expression of γH2AX in response to DNA damage and might be a promising anti-cancer drug candidate for the treatment of oral cancer.

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Section: Discussionmentioning

confidence: 98%

Oridonin induces apoptosis in human oral cancer cells via phosphorylation of histone H2AX

Yang

Shin

Lee

et al. 2017

European J Oral Sciences

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show abstract

“…Studies have shown that Oridonin can specifically inhibit NLRP3 inflammasome activation, where NACHT domain and Oridonin share cysteine 279 binding site ( 114 ). The ability of Oridonin to suppress cell proliferation was previously demonstrated in breast ( 133 ) ovarian ( 115 ) and esophageal ( 116 ) cancers. On the other hand, CY-09 ( 117 ), OLT1177( 118 , 119 ), Tranilast ( 120 , 121 ) present as promising specific NLRP3 inhibitors.…”

Section: Therapeutic Potential Of Targeting Nlrp3 Inflammasome In Canmentioning

confidence: 88%

NLRP3 Inflammasome Activation in Cancer: A Double-Edged Sword

2020

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Inflammation is involved in tumor development and progression as well as antitumor response to therapy. In the past decade, the crosstalk between inflammation, immunity, and cancer has been investigated extensively, which led to the identification of several underlying mechanisms and cells involved. The formation of inflammasome complexes leads to the activation of caspase-1, production of interleukin (IL)-1β, and IL-18 and pyroptosis. Multiple studies have shown the involvement of NLRP3 inflammasome in tumorigenesis. Conversely, other reports have indicated a protective role in certain cancers. In this review, we summarize these contradictory roles of NLRP3 inflammasome in cancer, shed the light on oncogenic signaling leading to NLRP3 activation and IL-1β production and outline the current knowledge on therapeutic approaches.

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“…CCL18 induced OC invasiveness is strongly connected with mTORC2 [ 69 ]. Blockage of mTOR signaling results in suppression of proliferation of OC [ 70 ]. mTOR increases OC cells viability and decreases their apoptosis and autophagy [ 71 ].…”

Section: Interrelation Of Pi3k/akt/mtor and Pim Pathways In Ovariamentioning

confidence: 99%

PIM Kinases and Their Relevance to the PI3K/AKT/mTOR Pathway in the Regulation of Ovarian Cancer

et al. 2018

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Ovarian cancer is a medical term that includes a number of tumors with different molecular biology, phenotypes, tumor progression, etiology, and even different diagnosis. Some specific treatments are required to address this heterogeneity of ovarian cancer, thus molecular characterization may provide an important tool for this purpose. On a molecular level, proviral-integration site for Moloney-murine leukemia virus (PIM) kinases are over expressed in ovarian cancer and play a vital role in the regulation of different proteins responsible for this tumorigenesis. Likewise, the phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) pathway is also a central regulator of the ovarian cancer. Interestingly, recent research has linked the PIM kinases to the PI3K/AKT/mTOR pathway in several types of cancers, but their connection in ovarian cancer has not been studied yet. Once the exact relationship of PIM kinases with the PI3K/AKT/mTOR pathway is acquired in ovarian cancer, it will hopefully provide effective treatments on a molecular level. This review mainly focuses on the role of PIM kinases in ovarian cancer and their interactions with proteins involved in its progression. In addition, this review suggests a connection between the PIM kinases and the PI3K/AKT/mTOR pathway and their parallel mechanism in the regulation of ovarian cancer.

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Oridonin Suppresses Proliferation of Human Ovarian Cancer Cells via Blockage of mTOR Signaling

Cited by 18 publications

References 19 publications

Oridonin induces apoptosis in human oral cancer cells via phosphorylation of histone H2AX

Oridonin induces apoptosis in human oral cancer cells via phosphorylation of histone H2AX

NLRP3 Inflammasome Activation in Cancer: A Double-Edged Sword

PIM Kinases and Their Relevance to the PI3K/AKT/mTOR Pathway in the Regulation of Ovarian Cancer

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