Baicalein inhibits the migration and invasion of colorectal cancer cells via suppression of the AKT signaling pathway

Rui, Xiaojiang; Yan, Xin; Zhang, Kai

doi:10.3892/ol.2015.3935

Cited by 43 publications

(75 citation statements)

References 26 publications

(32 reference statements)

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“…Previous studies demonstrated that baicalein could exert its anti-tumor effect through modulating the PI3K/AKT signaling pathway in several cancer types [26-28]. To explore the effect of baicalein on PI3K/AKT pathway, the phosphorylation level of AKT at Thr308 and Ser473 in Bel-7402 cells treated with 0, 40 and 80 µM baicalein for 24 h was detected by western blotting, we found the phosphorylation level of AKT at both Thr308 and Ser473 were significantly decreased by baicalein treatment (Fig.…”

Section: Resultsmentioning

confidence: 99%

Baicalein, a Natural Anti-Cancer Compound, Alters MicroRNA Expression Profiles in Bel-7402 Human Hepatocellular Carcinoma Cells

Bie

Sun

et al. 2017

Cell Physiol Biochem

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Background/Aims: Baicalein has been shown to possess significant anti-hepatoma activity by inhibiting cell proliferation. Whether the anti-proliferative effect of baicalein is related to its modulation of miRNA expression in hepatocellular carcinoma (HCC) is still unknown. Methods: The anti-proliferative effects of baicalein on HCC cell line Bel-7402 was assessed by detecting the proliferation activity, cell cycle distribution, expression changes of p21/CDKN1A, P27/CDKN1B, total Akt and phosphoryted AKT. Microarray analysis was conducted to determine the miRNA expression profiles in baicalein-treated or untreated Bel-7402 cells and then validated by qRT-PCR in two HCC cell lines (Bel-7402 and Hep3B). The gain-of-function of miR-3127-5p was performed by detecting anti-proliferative effects after transfecting miRNA mimics in cells. Finally, the expression level of miR-3127-5p in different HCC cell lines was determined by qRT-PCR. Results: Baicalein was able to inhibit the proliferation of Bel-7402 cells by inducing cell cycle arrest at the S and G2/M phase via up-regulating the expression of p21/CDKN1A and P27/CDKN1B and suppressing the PI3K/Akt pathway. Baicalein could alter the miRNA expression profiles in Bel-7402 cells. Putative target genes for differentially expressed miRNAs could be enriched in terms of cell proliferation regulation, cell cycle arrest and were mainly involved in MAPK, PI3K-Akt, Wnt, Hippo and mTOR signaling pathways. MiR- 3127-5p, one of up-regulated miRNAs, exhibits low expression level in several HCC cell lines and its overexpression could inhibit cell growth of Bel-7402 and Hep3B cell lines by inducing S phase arrest by up-regulating the expression of p21and P27 and repressing the PI3K/Akt pathway. Conclusions: Modulation of miRNA expression may be an important mechanism underlying the anti-hepatoma effects of baicalein.

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Section: Resultsmentioning

confidence: 99%

Baicalein, a Natural Anti-Cancer Compound, Alters MicroRNA Expression Profiles in Bel-7402 Human Hepatocellular Carcinoma Cells

Bie

Sun

et al. 2017

Cell Physiol Biochem

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“…Both MMP-2 and MMP-9 are crucial proteases for the invasion and migration of CRC cells. Treatment of CRC cells with baicalein significantly inhibited cellular migration and invasion by suppressing the activities of MMP-2 and MMP-9 (via inhibition of the Akt pathway) [12]. Another group looked at the effect of baicalein on DLD-1 cells (colorectal adenocarcinoma cells) using proteomic analysis.…”

Section: Baicalein and Colorectal Cancermentioning

confidence: 99%

“…Baicalein is a flavone and an active ingredient in the traditional herb, Huang Qin. There is an accumulating amount of evidence that demonstrates baicalein’s role in treating and preventing various types of cancer [9,10,11,12,13,14,15]. In this review, we explored its chemical structure, properties, and possible biological mechanisms through which it acts.…”

Section: Introductionmentioning

confidence: 99%

The Fascinating Effects of Baicalein on Cancer: A Review

Liu

Dong

Gao

et al. 2016

IJMS

188

133

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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.

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“…Our study also showed that downregulation of CPEB4 increased level of cellular ROS, which may result in decreasing p‐Akt levels. Akt phosphorylation signal may contribute to cancer cells functioning, such as viability (Tang et al, ), proliferation (Zhou et al, ), invasion (Rui et al, ) and migration (Wang et al, ; Zhou et al, ). In the present study, our data indicated PI3 K/Akt inhibitor, LY294002, which effectively suppressed siCPEB4 suppresses cell migration and invasion of NSCLC cells.…”

Section: Discussionmentioning

confidence: 99%

Knockdown of CPEB4 expression suppresses cell migration and invasion via Akt pathway in non‐small cell lung cancer

Zhang

Chen

et al. 2018

Cell Biology International

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Cytoplasmic polyadenylation element binding protein 4 (CPEB4) could be an important regulator in variety of cancers. However, the biological function and the underlying molecular mechanism of CPEB4 in non-small cell lung cancer (NSCLC) remains unknown. In this study, we investigated the metastasis role of CPEB4 in NSCLC cells, we knocked down CPEB4 using siRNA. Transwell migration assay and cell invasion assay on Matrigel were presented, and cell migration was also determined by scratch-healing assay. ROS generation were determined by fluorescence probe DCFH2-DA. The protein expression was assessed by ELISA and Western blot analysis. LY294002 were used to inhibit PI3 K/Akt signaling. The data showed that knockdown of CPEB4 inhibited the migration and invasion of NSCLC. Moreover, silencing of CPEB4 reduced Snail and MMP-3 expression in vitro. We also indicated that CPEB4 knockdown increased the ROS expression. Furthermore, we found that silencing of CPEB4 decreased pAkt expression. Taken all together, our data demonstrated that silencing of CPEB4 induces ROS generation, thus suppressing the Akt expression, which finally prevents NSCLC cells invasion and migration. Therefore, CPEB4 may regard as a target to inhibit NSCLC invasion and metastasis through Akt pathway.

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Baicalein inhibits the migration and invasion of colorectal cancer cells via suppression of the AKT signaling pathway

Cited by 43 publications

References 26 publications

Baicalein, a Natural Anti-Cancer Compound, Alters MicroRNA Expression Profiles in Bel-7402 Human Hepatocellular Carcinoma Cells

Baicalein, a Natural Anti-Cancer Compound, Alters MicroRNA Expression Profiles in Bel-7402 Human Hepatocellular Carcinoma Cells

The Fascinating Effects of Baicalein on Cancer: A Review

Knockdown of CPEB4 expression suppresses cell migration and invasion via Akt pathway in non‐small cell lung cancer

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