Centipeda minima (Ebushicao) extract inhibits PI3K-Akt-mTOR signaling in nasopharyngeal carcinoma CNE-1 cells

Guo, Yu; Hai, Sun; Chan, Chi-On; Liu, Bei Bei; Wu, Jian; Chan, Shun Wan; Mok, Daniel K. W.; Tse, Anfernee Kai-Wing; Yu, Zhi Ling; Chen, Sibao

doi:10.1186/s13020-015-0058-5

Cited by 26 publications

(33 citation statements)

References 29 publications

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“…As is known to all, Akt/mTOR signaling pathway participates in multiple cellular functions, including cell survival, differentiation, and autophagy [ 20 ].The Akt/mTOR signaling pathway could negatively regulate autophagy through Akt phosphorylation, following by promoting phosphorylation and activation of mTOR [ 21 , 22 ]. Notably, SMI-4a could down-regulate the phosphorylation level of Akt and mTOR.…”

Section: Discussionmentioning

confidence: 99%

Ginsenoside G-Rh2 synergizes with SMI-4a in anti-melanoma activity through autophagic cell death

Chen

Ding

et al. 2018

Chin Med

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BackgroundMelanoma is a leading cause of cancer death worldwide, and SMI-4a and G-Rh2 exert anti-tumor activity in multiple cancer. However, SMI-4a as well as a synergistic relationship between SMI-4a and G-Rh2 in anti-melanoma capacity are still unknown. Therefore, we investigated the effects of SMI-4a and combined SMI-4a with G-Rh2 on the viability, apoptosis and autophagy of melanoma, and to preliminarily explore the underlying mechanism of SMI-4a and combined SMI-4a with G-Rh2 in inhibiting tumor growth.MethodsCell viability was examined with cell counting Kit 8 assay and colony formation assay; Apoptosis was evaluated by flow cytometry and Caspase 3/7 activity assay; Western blotting was used to test proteins related to autophagy and the AKT/mammalian target of rapamycin (mTOR) signaling pathway; Tumor xenograft model in BALB/c nude mice was performed to evaluate the effects of SMI-4a and combined SMI-4a with G-Rh2 in anti-melanoma in vivo.ResultsSMI-4a, a pharmacological inhibitor of PIM-1, could decrease cell viability, induce apoptosis, and promote Caspase 3/7 activity in both A375 and G361 melanoma cells, and SMI-4a inhibited tumor growth by inducing autophagy via down-regulating AKT/mTOR axis in melanoma cells. Furthermore, G-Rh2 amplified the anti-tumor activity of SMI-4a in melanoma cells via strengthening autophagy.ConclusionsOur results suggested that SMI-4a could enhance autophagy-inducing apoptosis by inhibiting AKT/mTOR signaling pathway in melanoma cells, and G-Rh2 could enhance the effects of SMI-4a against melanoma cancer via amplifying autophagy induction. This study demonstrates that combined SMI-4a and G-Rh2 might be a novel alternative strategy for melanoma treatment.Electronic supplementary materialThe online version of this article (10.1186/s13020-018-0168-y) contains supplementary material, which is available to authorized users.

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Section: Discussionmentioning

confidence: 99%

Ginsenoside G-Rh2 synergizes with SMI-4a in anti-melanoma activity through autophagic cell death

Chen

Ding

et al. 2018

Chin Med

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“…As previously described (22,27), Centipeda minima was collected in August 2010 in Xiangfan, Hubei Province, China (latitude, 32 • 04 ′ N; longitude, 112 • 05 ′ E), and authenticated by Prof. Sibao Chen based on morphological features. A voucher specimen (EBSC-016-09) was deposited at the herbarium of the State Key Laboratory of Chinese Medicine and Molecular Pharmacology, Department of Applied Biology and Chemical Technology, The Hong Kong Polytechnic University.…”

Section: Plant Materials and Sample Preparationmentioning

confidence: 99%

“…Reports suggest that Centipeda minima extracts (CME) possess anti-inflammatory (17), anti-bacterial (18,19), and anti-allergic (20) effects. Previous studies have demonstrated the anti-cancer effects of CME, and compounds extracted from CM, in various cancers including nasopharyngeal carcinoma (13,14,21,22), leukemia (23), glioblastoma (24), lung cancer (25), and colon cancer (26), however, the effects of CME on breast cancer have to date, not been demonstrated.…”

Section: Introductionmentioning

confidence: 99%

Anti-cancer Activity of Centipeda minima Extract in Triple Negative Breast Cancer via Inhibition of AKT, NF-κB, and STAT3 Signaling Pathways

et al. 2020

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Breast cancer is the most commonly diagnosed cancer in females worldwide. Estimates from the World Health Organization (WHO) International Agency for Research on Cancer, suggest that globally, there were around 2.1 million new breast cancer cases and 627,000 deaths due to breast cancer in 2018. Among the subtypes of breast cancer, triple negative breast cancer (TNBC) is the most aggressive and carries the poorest prognosis, largest recurrence, and lowest survival rate. Major treatment options for TNBC patients are mainly constrained to chemotherapy, which can be accompanied by severe side effects. Therefore, development of novel and effective anti-cancer drugs for the treatment of TNBC are urgently required. Centipeda minima is a well-known traditional Chinese herbal medicine that has historically been used to treat rhinitis, sinusitis, relieve pain, and reduce swelling. Recent studies have shown that Centipeda minima exhibited efficacy against certain cancers, however, to date, no studies have been conducted on its effects in breast cancer. Here, we aimed to investigate the anti-cancer activity of the total extract of Centipeda minima (CME), and its underlying mechanism, in TNBC. In MDA-MB-231, we found that CME could significantly reduce cell viability and proliferation, induce apoptosis and inhibit cancer cell migration and invasion, in a dose and time-dependent manner. We showed that CME may potentially act via inhibition of multiple signaling pathways, including the EGFR, PI3K/AKT/mTOR, NF-κB, and STAT3 pathways. Treatment with CME also led to in vitro downregulation of MMP-9 activity and inhibition of metastasis. Further, we demonstrated that CME could significantly reduce tumor burden in MDA-MB-231 xenograft mice, without any appreciable side effects. Based on our findings, CME is a promising candidate for development as a therapeutic with high efficacy against TNBC.

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“…How to reduce the toxicity and side effects of anti-cancer drugs has become a major problem that we need to solve urgently. In recent years, the research on the prevention and treatment of NPC by traditional Chinese medicine is popular year by year, and these traditional Chinese medicines have achieved satisfactory results [2][3][4].…”

Section: Introductionmentioning

confidence: 99%

Junduqing extractive promotes the apoptosis of nasopharyngeal carcinoma cells through down-regulating Mcl-1 and Bcl-xL and up-regulating Caspase-3, Caspase-8 and Caspase-9

Zhao

Tang

Gao

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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This study aimed to investigate the effect of Junduqing extractive on proliferation, apoptosis, migration and invasion of nasopharyngeal carcinoma (NPC) cells and the involved mechanism. Junduqing extractive was prepared. CCK-8 assay found that IC50 of Junduqing extractive in HNE-1 cells was 2.99 mg/ml, so its concentration of 1.0, 2.0 and 3.0 mg/ml was selected to perform the following experiments. HNE-1, HNE-2 and HONE1 cells were then divided into four groups: (1) Control (no treatment); (2) 1.0 mg/ml (1.0 mg/ml Junduqing); (3) 2.0 mg/ml (2.0 mg/ml Junduqing) and (4) 3.0 mg/ml (3.0 mg/ml Junduqing). Cell viability, apoptosis, migration and invasion were examined by CCK-8 assay, annexin V-FITC/PI staining, scratch wound assay and transwell assay, respectively. Compared with the control group, the viability, migration rates and invasive capacity of HNE-1, HNE-2 and HONE1 cells with Junduqing treatments decreased significantly. Higher concentration of Junduqing extractive caused lower viability, smaller migration rates and weaker invasive capacity. Compared with the control group, the apoptosis of HNE-1, HNE-2 and HONE1 cells after treatment with 2.0 and 3.0 mg/ml of Junduqing extractive increased remarkably. Levels of Bcl-xL, Mcl-1, Caspase-3, Caspase-8 and Caspase-9 were examined by western blotting. Compared with the control group, the expression of Bcl-xL and Mcl-1 and the expression of Caspase-3, Caspase-8 and Caspase-9 in HNE-1, HNE-2 and HONE1 cells were significantly downregulated and up-regulated, respectively, after treatment with Junduqing extractive. In conclusion, Junduqing extractive could inhibit the proliferation, migration and invasion, and promote the apoptosis of human NPC cells through down-regulating Mcl-1 and Bcl-xL and up-regulating Caspase-3, Caspase-8 and Caspase-9.

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Centipeda minima (Ebushicao) extract inhibits PI3K-Akt-mTOR signaling in nasopharyngeal carcinoma CNE-1 cells

Cited by 26 publications

References 29 publications

Ginsenoside G-Rh2 synergizes with SMI-4a in anti-melanoma activity through autophagic cell death

Ginsenoside G-Rh2 synergizes with SMI-4a in anti-melanoma activity through autophagic cell death

Anti-cancer Activity of Centipeda minima Extract in Triple Negative Breast Cancer via Inhibition of AKT, NF-κB, and STAT3 Signaling Pathways

Junduqing extractive promotes the apoptosis of nasopharyngeal carcinoma cells through down-regulating Mcl-1 and Bcl-xL and up-regulating Caspase-3, Caspase-8 and Caspase-9

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