Huaier Aqueous Extract Induces Hepatocellular Carcinoma Cells Arrest in S Phase via JNK Signaling Pathway

Zhang, Chengshuo; Zhang, Jialin; Li, Xin; Sun, Ning; Yu, Rui; Zhao, Baisong; Yu, Dongyang; Cheng, Ying; Liu, Yongfeng

doi:10.1155/2015/171356

Cited by 20 publications

(22 citation statements)

References 29 publications

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“…We think the roles of the ERK and p38 are partly associated with cell type. On the contrary, JNK signaling pathway was considered to induce HCC cell cycle arrest and induced HCC apoptosis (27). In the present study we also found that emodin may suppress the activation of JNK mildly, this indicates the JNK pathway may not play a major role in emodin's effect.…”

Section: Discussionsupporting

confidence: 38%

Emodin induces hepatocellular carcinoma cell apoptosis through MAPK and PI3K/AKT signaling pathways in vitro and in vivo

et al. 2016

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Abstract. Emodin is an active ingredient derived from root and rhizome of Rheum palmatum L and many studies have reported that it exhibits anticancer effects in a number of human tumors. However, there is little information demonstrating the possible effects of emodin on the proliferation and apoptosis of hepatocellular carcinoma (HCC). In the present study, we show that emodin may inhibit the proliferation of SMMC-7721 cells in a dose-and time-dependent manner and induced apoptosis of cells in a concentration-dependent manner after treatment for 24 h. Moreover, we further discovered that the possible molecular mechanisms involved may relate to the mitogenactivated protein kinase (MAPK) and phosphoinositide 3-kinase (PI3K)/AKT signaling pathways. Emodin may induce the phosphorylation of extracellular-signal-regulated kinase (ERK) and p38 while mildly suppressed the expression of p-c-Jun-N-terminal kinase (p-JNK). However, emodin did not affect the expression of the total (t)-ERK, t-p38 or t-JNK. Furthermore, emodin also suppressed the activation of p-AKT, but not the t-AKT. In vivo, we found that emodin suppressed tumor growth in experimental mice without an obvious change in body weight, which may work through the antiproliferation and apoptosis inducing effects. Moreover, emodin improves the liver and kidney function in mice, revealing that emodin may improve the life quality of the mice with implanted tumors. In conclusion, the above findings indicate that emodin may be a potentially effective and safe drug to induce apoptosis of HCC.

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Section: Discussionsupporting

confidence: 38%

Emodin induces hepatocellular carcinoma cell apoptosis through MAPK and PI3K/AKT signaling pathways in vitro and in vivo

et al. 2016

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“…Recently, increasing attentions have been paid to anti-tumor drugs originating from TCM 7 . A lot of clinical applications have revealed that Huaier has a good anti-tumor activity, especially in HCC 27 28 29 . Nevertheless, the underlying mechanisms of anti-HCC effect of Huaier remain ill defined.…”

Section: Discussionmentioning

confidence: 99%

“…Our result was consistent with a previous finding that Huaier suppressed cell viability and induced G0/G1 cell-cycle arrest in breast cancer cell lines 12 . However, there are several studies reporting that Huaier induced cell-cycle arrest in G2/M phase in human cervical cancer cells 30 and human melanoma cells 31 , and caused S phase arrest in human hepatocellular carcinoma cell lines HepG2 and Bel-7402 28 . This phenomenon may be interpreted by the complicated effects of Huaier on different cell lines.…”

Section: Discussionmentioning

confidence: 99%

Huaier restrains proliferative and invasive potential of human hepatoma SKHEP-1 cells partially through decreased Lamin B1 and elevated NOV

Yang

et al. 2016

Sci Rep

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Hepatocellular carcinoma (HCC) is one of the most common cause of malignancy-related mortality worldwide. It is urgently needed to develop potential drugs with good efficacy and low toxicity for HCC treatment. The anti-tumor effect of Traditional Chinese Medicine (TCM) has received increasing attention worldwide. Trametes robiniophila Murr. (Huaier) has been used in TCM for approximately 1,600 years. Clinically, Huaier has satisfactory therapeutic effects in cancer treatment, especially in HCC. However, the mechanisms underlying the anti-cancer effect of Huaier remain ill defined. Herein we have demonstrated that Huaier dramatically inhibited cell proliferation and induced apoptosis in human hepatoma cell line SKHEP-1. Importantly, Huaier restrained the metastatic capability of SKHEP-1 cells. Mechanistically, down-regulation of Lamin B1 and up-regulation of Nephroblastoma overexpressed (NOV) were at least partially responsible for the inhibitory effect of Huaier on the proliferative and invasive capacity of SKHEP-1 cells. Our finding provided new insights into mechanisms of anti-HCC effect of Huaier and suggested a new scientific basis for clinical medication.

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“…Wang X et al and Zhang N et al reported that cellcycle arrest occurs in breast cancer MCF-7 and MDA-MB-231 cells and human umbilical vein endothelial cells in the G0/G1 phase [16,31]. Zhang C found that Huaier extract induces hepatocellular carcinoma cell HepG2 and Bel-7402 arrest in S phase [32]. In conclusion, Huaier extract causes cell apoptosis and induces cancer cell arrest in different phases.…”

Section: Cellular Physiology and Biochemistrymentioning

confidence: 91%

Huang Qi Huai Granules Induce Apoptosis in Acute Lymphoblastic Leukemia Cells through the Akt/FoxO1 Pathway

Han¹,

Lin²,

Zeng³

et al. 2016

Cell Physiol Biochem

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Background/Aims: In recent years, a traditional Chinese medicine named Huang Qi Huai (HQH) has been frequently used in China for solid tumor therapy. However, the role of HQH on leukemia cells and its underlying mechanisms have not been elucidated. In this study, we investigated the effect of HQH on the proliferation and apoptosis of acute lymphoblastic leukemia (ALL) cell lines. Methods: Sup-B15 and Nalm-6 cells were treated with gradient doses of HQH for 24, 48 or 72 h. Cell viability was measured using a CCK8 assay and cell cycle distribution and apoptosis levels were analyzed using flow cytometry. Western blotting was used to assess the levels of proteins associated with the apoptotic pathway. Results: The results revealed that cell survival decreased significantly with increasing concentrations of HQH. HQH induced G2 cell-cycle arrest and cell apoptosis in a dose-dependent manner. HQH inhibited phosphorylated-Akt, phosphorylated- FoxO1 and Bcl2 expression and upregulated Bim, cleaved-caspase-3 and Bax expression in a dose-dependent manner, which suggests that HQH induces the apoptosis of ALL cells via the Akt/FoxO1 pathway. Conclusion: HQH is a potential complementary agent for the treatment of acute lymphoblastic leukemia.

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Huaier Aqueous Extract Induces Hepatocellular Carcinoma Cells Arrest in S Phase via JNK Signaling Pathway

Cited by 20 publications

References 29 publications

Emodin induces hepatocellular carcinoma cell apoptosis through MAPK and PI3K/AKT signaling pathways in vitro and in vivo

Emodin induces hepatocellular carcinoma cell apoptosis through MAPK and PI3K/AKT signaling pathways in vitro and in vivo

Huaier restrains proliferative and invasive potential of human hepatoma SKHEP-1 cells partially through decreased Lamin B1 and elevated NOV

Huang Qi Huai Granules Induce Apoptosis in Acute Lymphoblastic Leukemia Cells through the Akt/FoxO1 Pathway

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