Baicalein inhibits the invasion of gastric cancer cells by suppressing the activity of the p38 signaling pathway

Yan, Xin; Rui, Xiaojiang; Zhang, Kai

doi:10.3892/or.2014.3669

Cited by 51 publications

(30 citation statements)

References 26 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Signaling pathways are involved in its function of anti-CRC, including activation of the Nrf2 signaling pathway [27] and attenuation of the MAPKs and PI3K-Akt activation [28]. As for other common malignant tumors, several reports have revealed various kinds of signal paths mediated by baicalein [8,29,30]. In the most important part of our research, we examined the proliferation of HCT116 cell periods by CCK-8 assay and flow cytometry (FCM).…”

Section: Discussionmentioning

confidence: 99%

Baicalein Inhibits Proliferation Activity of Human Colorectal Cancer Cells HCT116 Through Downregulation of Ezrin

Chen

Hou

Gao

et al. 2018

Cell Physiol Biochem

View full text Add to dashboard Cite

Background/Aims: The present study was aimed at examining Ezrin expression in human colorectal cancer (CRC) tissues and elucidating the influence of baicalein on the proliferation of HCT116 cells. Methods: The expression of Ezrin was determined by qRT-PCR and immunohistochemistry. HCT116 cells were divided into four groups－ baicalein groups with various concentrations, pcDNA3.1-Ezrin group, si-Ezrin group and dual inhibitory group (baicalein + si-Ezrin). CCK-8 assay and flow cytometry (FCM) were employed to assess cell proliferation and to detect the distribution of cell cycle respectively. The expression levels of Ezrin protein and cell cycle-associated proteins were detected by using western blot. The proliferation ability of CRC cells was also evaluated in vivo. Results: Ezrin expression in CRC tissues was observably higher than that in adjacent colorectal tissues. With drug concentration and action time of baicalein increasing, the cell propagation capacity of HCT116 cells was decreased and the cell cycle progression was arrested. Ezrin expression was inhibited by the administration of baicalein in a dose-dependent way. The levels of CyclinD1 and CDK4 were also significantly decreased, but the expression of P53 pathway proteins P53 and P21 was markedly upregulated. Conclusion: Baicalein repressed proliferation of human colorectal cancer cells HCT116 and blocked cell cycle through downregulating Ezrin and upregulating P53 pathway-related proteins.

show abstract

Section: Discussionmentioning

confidence: 99%

Baicalein Inhibits Proliferation Activity of Human Colorectal Cancer Cells HCT116 Through Downregulation of Ezrin

Chen

Hou

Gao

et al. 2018

Cell Physiol Biochem

View full text Add to dashboard Cite

show abstract

“…This study provided the basic mechanism for baicalein’s inhibition of metastasis in gastric cancer cells by inactivation of the TGF-β/Smad4 pathway [43]. Similarly, another study revealed that baicalein inhibited the invasion of gastric cancer cells by inhibition of the p38 signaling pathway and subsequent MMP-2 and MMP-9 suppression [44]. Baicalein was reported to reverse hypoxia-induced 5-FU resistance in gastric cancer AGS cells.…”

Section: Baicalein and Gastric Cancermentioning

confidence: 99%

The Fascinating Effects of Baicalein on Cancer: A Review

Liu

Dong

Gao

et al. 2016

IJMS

189

133

View full text Add to dashboard Cite

Cancer is one of the leading causes of death worldwide and a major global health problem. In recent decades, the rates of both mortality and morbidity of cancer have rapidly increased for a variety of reasons. Despite treatment options, there are serious side effects associated with chemotherapy drugs and multiple forms of drug resistance that significantly reduce their effects. There is an accumulating amount of evidence on the pharmacological activities of baicalein (e.g., anti-inflammatory, antioxidant, antiviral, and antitumor effects). Furthermore, there has been great progress in elucidating the target mechanisms and signaling pathways of baicalein’s anti-cancer potential. The anti-tumor functions of baicalein are mainly due to its capacities to inhibit complexes of cyclins to regulate the cell cycle, to scavenge oxidative radicals, to attenuate mitogen activated protein kinase (MAPK), protein kinase B (Akt) or mammalian target of rapamycin (mTOR) activities, to induce apoptosis by activating caspase-9/-3 and to inhibit tumorinvasion and metastasis by reducing the expression of matrix metalloproteinase-2/-9 (MMP-2/-9). In this review, we focused on the relevant biological mechanisms of baicalein involved in inhibiting various cancers, such as bladder cancer, breast cancer, and ovarian cancer. Moreover, we also summarized the specific mechanisms by which baicalein inhibited the growth of various tumors in vivo. Taken together, baicalein may be developed as a potential, novel anticancer drug to treat tumors.

show abstract

“…The mitogen-activated protein kinase (MAPK) signaling pathway is widely expressed in multicellular organisms, with critical roles in multiple biological processes, such as cell proliferation, migration, and invasion. The function of the three central kinases of the MAPK signaling pathway, ERK, JNK and p38 were all involved in the metastasis and invasion of gastric cancer [36–39]. …”

Section: Discussionmentioning

confidence: 99%

Asparaginyl endopeptidase promotes the invasion and metastasis of gastric cancer through modulating epithelial-to-mesenchymal transition

Cui

Wang

et al. 2016

Oncotarget

View full text Add to dashboard Cite

Asparaginyl endopeptidase (AEP) is a lysosomal protease often overexpressed in gastric cancer. AEP was expressed higher in peritoneal metastatic loci than in primary gastric cancer. Then we overexpressed AEP or knocked it down with a lentiviral vector in gastric cancer cell lines and detected the cell cycle arrest and the changes of the invasive and metastatic ability in vitro and in vivo. When AEP was knocked-down, the proliferative, invasive and metastatic capacity of gastric cancer cells were inhibited, and the population of sub-G1 cells increased. AEP knockdown led to significant decrease of expression of transcription factor Twist and the mesenchymal markers N-cadherin, ß-catenin and Vimentin and to increased expression of epithelial marker E-cadherin. These results showed that AEP could promote invasion and metastasis by modulating EMT. We used phosphorylation-specific antibody microarrays to investigate the mechanism how AEP promotes gastric cancer invasion and metastasis, and found that the phosphorylation level of AKT and MAPK signaling pathways was decreased significantly if AEP was knocked-down. Therefore, AKT and MAPK signaling pathways took part in the modulation.

show abstract

Baicalein inhibits the invasion of gastric cancer cells by suppressing the activity of the p38 signaling pathway

Cited by 51 publications

References 26 publications

Baicalein Inhibits Proliferation Activity of Human Colorectal Cancer Cells HCT116 Through Downregulation of Ezrin

Baicalein Inhibits Proliferation Activity of Human Colorectal Cancer Cells HCT116 Through Downregulation of Ezrin

The Fascinating Effects of Baicalein on Cancer: A Review

Asparaginyl endopeptidase promotes the invasion and metastasis of gastric cancer through modulating epithelial-to-mesenchymal transition

Contact Info

Product

Resources

About