Ginsenoside 20(S)-Rg3 induced autophagy to inhibit migration and invasion of ovarian cancer

Zheng, Xia; Chen, Wei; Hou, Huilian; Li, Jie; Li, Huijin; Sun, Xun; Zhao, Le; Xu, Li

doi:10.1016/j.biopha.2016.11.072

Cited by 47 publications

(32 citation statements)

References 47 publications

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“…Numerous ginsenosides have been reported to be important regulators of autophagy and exert various biological activities either by inducing autophagy or by inhibiting autophagy. The ginsenosides that serve as autophagy inducer include CK, Rg3, Rh2, Rg1, Rg2, and F2 . Meanwhile, the ginsenosides that can inhibit autophagy include Ro, Rg3, Rg1, and Rb1 (Fig.…”

Section: Cellular Stress Response Mechanisms Regulated By Ginsenosidesmentioning

confidence: 99%

“…In addition, autophagy also impairs tumor metastasis. Autophagy induced by 20( S )‐Rg3 slightly antagonized the inhibitory effect of 20( S )‐Rg3 on cell viability, but dramatically promoted the inhibition of ovarian cancer cell migration and invasion; (2) protective autophagy concomitantly induced by cancer chemotherapeutics could be blocked by ginsenosides, which can overcome resistance and sensitize cancer cells to death. Doxorubicin‐induced autophagy plays a protective role in hepatocellular carcinoma (HCC) cells.…”

Section: Cellular Stress Response Mechanisms Regulated By Ginsenosidesmentioning

confidence: 99%

“…Autophagy can also be inhibited by ginsenosides (black) in at least two ways, one involving suppression of AMPK and activation of mTOR and the other involving blockage of autophagosome-lysosome fusion inducing autophagy or by inhibiting autophagy. The ginsenosides that serve as autophagy inducer include CK, 32,[134][135][136] Rg3, [137][138][139] Rh2, 137,[140][141][142] Rg1, 116 Rg2, 143 and F2. 144 Meanwhile, the ginsenosides that can inhibit autophagy include Ro, 145 Rg3, 146 Rg1, 35,[147][148][149] and Rb1 73 (Fig.…”

Section: Autophagy Pathway and The Effect Of Ginsenosidesmentioning

confidence: 99%

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Cellular stress response mechanisms as therapeutic targets of ginsenosides

2017

Medicinal Research Reviews

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Ginseng, one of the most widely used traditional herbal medicines and dietary supplements, has historically been recognized as a tonic herb and adaptogen that can enhance the body's tolerance to various adversities. Ginsenosides are a diverse group of steroidal saponins that comprise the major secondary metabolites of ginseng and are responsible for its multiple pharmacological effects. Emerging evidence suggests that hormetic phytochemicals produced by environmentally stressed plants can activate the moderate cellular stress response mechanisms at a subtoxic level in humans, which may enhance tolerance against severe dysfunction or disease. In this review, we initially describe the role of ginsenosides in the chemical defense of plants from the genus Panax suffering from biotic and abiotic stress. Next, we summarize the diverse evolutionarily conserved cellular stress response pathways regulated by ginsenosides and the subsequent stress tolerance against various dysfunctions or diseases. Finally, the structure-activity relationship involved in the effect of ginsenosides is also analyzed. The evidence presented in this review implicates that ginseng as "the King of all herbs" could be regarded as a well-characterized example of the critical role of cellular stress response mechanisms in understanding the health benefits provided by herbal medicines from an evolutionary and ecological perspective.

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Section: Cellular Stress Response Mechanisms Regulated By Ginsenosidesmentioning

confidence: 99%

Section: Cellular Stress Response Mechanisms Regulated By Ginsenosidesmentioning

confidence: 99%

Section: Autophagy Pathway and The Effect Of Ginsenosidesmentioning

confidence: 99%

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Cellular stress response mechanisms as therapeutic targets of ginsenosides

2017

Medicinal Research Reviews

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“…Autophagy is a negative regulator for NLRP3 inflammasome activation, 23 and induction of autophagy has been linked to Rg3. 24,25 Indeed, inhibition of autophagy by 3-MA enhanced nigericin-induced IL-1β secretion in LPS-primed THP-1 cells, but this enhancement did not change in the presence of Rg3 ( Figure 4D). Furthermore, Rg3 treatment did not significantly induce autophagy in THP-1 cells ( Figure 4E), which ruled out the possible role for autophagy in the inhibitory effect of Rg3 on the NLRP3 inflammasome activation.…”

Section: Ginsenoside Rg3 Has No Effect On Upstream Regulation Of Nlmentioning

confidence: 95%

Ginsenoside Rg3 suppresses the NLRP3 inflammasome activation through inhibition of its assembly

et al. 2019

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Ginsenoside Rg3 is one of the main constituents of Panax ginseng. Compelling evidence has demonstrated that ginsenoside Rg3 is capable of inhibiting inflammation.However, the mechanism mediating its anti-inflammatory effects remain unclear.Here we show that ginsenoside Rg3 blocks IL-1β secretion and caspase-1 activation through inhibiting LPS priming and the NLRP3 inflammasome activation in human and mouse macrophages. Rg3 specifically inhibits activation of NLRP3 but not the NLRC4 or AIM2 inflammasomes. In addition, Rg3 has no effect on upstream regulation of NLRP3 inflammasome, such as K + efflux, ROS production, or mitochondrial membrane potential. Mechanistically, Rg3 abrogates NEK7-NLRP3 interaction, and subsequently inhibits NLRP3-ASC interaction, ASC oligomerization, and speckle formation. More importantly, Rg3 can reduce IL-1β secretion induced by LPS in mice and protect mice from lethal endotoxic shock. Thus, our findings reveal an anti-inflammatory mechanism for Rg3 and suggest its potential use in NLRP3-driven diseases. K E Y W O R D Santi-inflammation, ginsenoside Rg3, inflammasome, NLRP3 inflammasome | 209 SHI et al. SUPPORTING INFORMATIONAdditional supporting information may be found online in the Supporting Information section.

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“…However, the specific function of Cx31 in thyroid cancer has been poorly understood. Ginsenoside (Rg1) is the main component of ginseng, which has been proven to be effective in the treatment of colon cancer, ovarian cancer and lung cancer [16–18]. Pharmacological studies have demonstrated that Rg1 can promote the apoptosis of tumor cells and enhance sensitization therapy of tumor cells [19,20].…”

Section: Introductionmentioning

confidence: 99%

Ginsenoside improves papillary thyroid cancer cell malignancies partially through upregulating connexin 31

Chen

et al. 2018

The Kaohsiung J of Med Scie

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Connexin 31 (Cx31) is considered a suppressor for many tumors. Ginsenoside (Rg1) is a traditional Chinese herb that is widely acknowledged due to its anti-tumor characteristics. However, limited studies have focused on the role of Rg1 in papillary thyroid cancer (PTC) cells. In the current study, we found that the expression of Cx31 in thyroid cancer tissues and thyroid cancer cell lines was significantly lower than that in normal thyroid epithelial tissues and cell lines. Overexpression of Cx31 reduced thyroid cancer cell proliferation, migration and invasion. Furthermore, we found that Rg1 significantly enhanced the expression of Cx31. Moreover, the proliferation and migration of IHH-4 and BCPAP cells were significantly reduced by Rg1 treatment. In contrast, the silencing of Cx31 enhanced the expression of Ki67 and proliferating cell nuclear antigen (PCNA). Meanwhile, treatment with Rg1 significantly decreased the protein levels of Ki67 and PCNA, but these effects could be abolished by transfection with si-Cx31. In summary, we provide novel evidence that the expression of Cx31 was decreased in thyroid cancer cells, but Rg1 treatment could significantly enhance the expression of Cx31 thereby suppressing thyroid cancer cell proliferation and migration.

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Ginsenoside 20(S)-Rg3 induced autophagy to inhibit migration and invasion of ovarian cancer

Cited by 47 publications

References 47 publications

Cellular stress response mechanisms as therapeutic targets of ginsenosides

Cellular stress response mechanisms as therapeutic targets of ginsenosides

Ginsenoside Rg3 suppresses the NLRP3 inflammasome activation through inhibition of its assembly

Ginsenoside improves papillary thyroid cancer cell malignancies partially through upregulating connexin 31

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