Blockade of epidermal growth factor receptor/mammalian target of rapamycin pathway by Icariside II results in reduced cell proliferation of osteosarcoma cells

Geng, Yadi; Yang, Lei; Zhang, Chao; Kong, Ling–Yi

doi:10.1016/j.fct.2014.08.002

Cited by 39 publications

(30 citation statements)

References 32 publications

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“…Meanwhile, the alternative mechanism has been proposed by another lab that blockade of EGFR/mTOR pathway resulted in the inhibition of cell proliferation in osteosarcoma (Geng et al. 2014 ). In prostate cancer cells, activation of cyclooxygenase-2/prostaglandin E2 pathway has been suggested to mediate baohuoside-I induced apoptosis (Lee et al.…”

Section: Discussionmentioning

confidence: 99%

Baohuoside-I suppresses cell proliferation and migration by up-regulating miR-144 in melanoma

Peng

Zhang

2017

Pharmaceutical Biology

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Context: Baohuoside-I was reported to induce apoptosis in non-small-cell lung cancer and inhibit the growth of multiple myeloma cells. The antitumour potential of baohuoside-I has not been demonstrated in melanoma yet.Objective: To investigate the potential antitumour activity of baohuoside-I against melanoma and elucidate its underlying molecular mechanism.Materials and methods: Cell viability was evaluated by MTT assay. The malignant invasion capacity was measured with trans-well assay. The relative expression change of microRNAs was profiled with microarray. TargetScan was utilized for prediction of target gene of miR-144. Regulatory effect of miR-144 on SMAD1 was determined by dual luciferase reporter assay. Endogenous SMAD1 protein in response to ectopic expression of miR-144 was determined by immunoblotting. Xenograft mice were employed to evaluate antitumour potential of baohuoside-I (25 mg/kg by tail intravenous injection every two days) in vivo.Results: Baohuoside-I significantly inhibited proliferation (45 ± 4% reduction in M14 and 35 ± 3% reduction in MV3 at 24 h) and migration (70 ± 4% reduction in M14 and 72 ± 3% reduction in MV3) in melanoma cells. Mechanistically, baohuoside-I up-regulated miR-144 expression levels (3 ± 0.2-fold). Silence of miR-144 reversed the inhibition of baohuoside-I in melanoma. We have identified that SMAD1 was the novel target of miR-144. Moreover, baohuoside-I suppressed melanoma in vivo (52 ± 8% reduction in xenograft tumour size at day 20).Conclusions: Our data suggested significant antitumour potential of baohuoside-I against melanoma both in vitro and in vivo, which warrants further laboratory investigation and clinical trial.

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Section: Discussionmentioning

confidence: 99%

Baohuoside-I suppresses cell proliferation and migration by up-regulating miR-144 in melanoma

Peng

Zhang

2017

Pharmaceutical Biology

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“…Icariside II has been investigated for its inhibitory effects on EGFR signaling in A431 human epidermoid carcinoma cells and in MG-63 and Saos-2 human osteosarcoma cells. Icariside II has demonstrated an inhibitory effect on EGFR expression and its downstream signaling molecules in all three cell lines which are discussed in detail in PI3K/AKT /mTOR and MAPK/ERK pathways 35 , 42 .…”

Section: Targeting Cancer Cells By Regulating Multiple Signaling Pmentioning

confidence: 92%

Targeting Apoptosis and Multiple Signaling Pathways with Icariside II in Cancer Cells

Khan¹,

Maryam²,

Qazi³

et al. 2015

Int. J. Biol. Sci.

120

119

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Cancer is the second leading cause of deaths worldwide. Despite concerted efforts to improve the current therapies, the prognosis of cancer remains dismal. Highly selective or specific blocking of only one of the signaling pathways has been associated with limited or sporadic responses. Using targeted agents to inhibit multiple signaling pathways has emerged as a new paradigm for anticancer treatment. Icariside II, a flavonol glycoside, is one of the major components of Traditional Chinese Medicine Herba epimedii and possesses multiple biological and pharmacological properties including anti-inflammatory, anti-osteoporosis, anti-oxidant, anti-aging, and anticancer activities. Recently, the anticancer activity of Icariside II has been extensively investigated. Here, in this review, our aim is to give our perspective on the current status of Icariside II, and discuss its natural sources, anticancer activity, molecular targets and the mechanisms of action with specific emphasis on apoptosis pathways which may help the further design and conduct of preclinical and clinical trials.Icariside II has been found to induce apoptosis in various human cancer cell lines of different origin by targeting multiple signaling pathways including STAT3, PI3K/AKT, MAPK/ERK, COX-2/PGE2 and β-Catenin which are frequently deregulated in cancers, suggesting that this collective activity rather than just a single effect may play an important role in developing Icariside II into a potential lead compound for anticancer therapy. This review suggests that Icariside II provides a novel opportunity for treatment of cancers, but additional investigations and clinical trials are still required to fully understand the mechanism of therapeutic effects to further validate it in anti-tumor therapy.

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“…In the present study, we discovered that EYK inhibitsmonomorphic malignant human glioma cell migration and invasion by downregulating MMP-9 activity and nuclear localization of NF-κB, the transcription factor primarily responsible for expression of MMP-9. Several studies have demonstrated that EYK has antitumor effects including reduction of drug resistance-causing gene mutations in lung cancer cells (24), induction of apoptosis in human prostate cancer cells (5) and non-small cell lung cancer (6), and downregulation of cell proliferation in osteosarcoma cells (25). However, this is the first study to demonstrate the ability of Cancer cell migration and invasion are the main biological characteristics associated with tumor malignancy (26).…”

Section: Discussionmentioning

confidence: 79%

Epimedium koreanum Nakai inhibits PMA-induced cancer cell migration and invasion by modulating NF-κB/MMP-9 signaling in monomorphic malignant human glioma cells

et al. 2017

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Previously, we showed that the herbal extract EYK (Epimedium koreanum Nakai) can regulate the immune response. Other studies showed that EYK has beneficial effects in human lung cancer, angiogenesis and Alzheimer's disease (AD). However, it remains unknown whether EYK can affect cancer cell migration and invasion in human brain cancer cell lines. In the present study, we found that pre- or post-treatment with EYK inhibited phorbol 12-myristate 13-acetate (PMA)-induced cancer cell migration and invasion in A172 cells, but not in U373MG or T98G cells. Additionally, pre- or post-treatment with PMA followed by EYK decreased MMP-9 activity in A172 cells. Moreover, treatment with a NF-κB inhibitor significantly decreased cell migration in A172 cells pre- or post-treated with EYK and PMA, suggesting that EYK requires NF-κB to alter cancer cell migration. Either pre- or post-treatment with EYK significantly decreased NF-κB nuclear translocation in comparison with PMA treatment. Taken together, our results suggest that EYK suppresses PMA-induced cancer cell migration in monomorphic malignant human glioma cells by downregulating the NF-κB pathway and decreasing MMP-9 activity.

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Blockade of epidermal growth factor receptor/mammalian target of rapamycin pathway by Icariside II results in reduced cell proliferation of osteosarcoma cells

Cited by 39 publications

References 32 publications

Baohuoside-I suppresses cell proliferation and migration by up-regulating miR-144 in melanoma

Baohuoside-I suppresses cell proliferation and migration by up-regulating miR-144 in melanoma

Targeting Apoptosis and Multiple Signaling Pathways with Icariside II in Cancer Cells

Epimedium koreanum Nakai inhibits PMA-induced cancer cell migration and invasion by modulating NF-κB/MMP-9 signaling in monomorphic malignant human glioma cells

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