Gallotannin regulates apoptosis and COX-2 expression via Akt and p38kinase pathway in human lung cancer cell line, A549

Yu, Seon Mi; Gweon, Eun Jeong; Chung, Ki Wha; Kim, Kwang Hoon; Cho, Hongsik; Kim, Song Ja

doi:10.1080/19768354.2012.696553

Cited by 9 publications

(7 citation statements)

References 44 publications

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“…Previous studies have also indicated the role of benzo(a)pyrene dihydrodiol epoxide, a byproduct of BAP, in the regulation of cell survival through microRNA-29a [71]. In line with our observations, treatment with nicotine was found to increase the clonogenic potential of various cancer cells [72,73]. In addition, silencing of Akt1 and 2 decreased the clonogenic efficiency of untreated and tobacco-treated cells.…”

Section: Discussionsupporting

confidence: 90%

“…Many previous studies have suggested the importance of Cox-2 in other cancers such as cancers of colorectal, breast, prostate, and blood. Moreover, in endometrial and lung cancer, Cox-2 was reported to be a downstream target of Akt and plays a significant role in the regulation of apoptosis of cancer cells [72,90,115,116]. In our study, we observed that the knockdown of both Akt1 and 2 isoforms led to the reduction of Cox-2 protein expression.…”

Section: Discussionsupporting

confidence: 62%

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Isoform-Specific Role of Akt in Oral Squamous Cell Carcinoma

et al. 2019

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Protein kinase B (Akt) plays a very significant role in various cancers including oral cancer. However, it has three isoforms (Akt1, Akt2, and Akt3) and they perform distinct functions and even play contrasting roles in different cancers. Therefore, it becomes essential to evaluate the isoform-specific role of Akt in oral cancer. In the present study, an attempt has been made to elucidate the isoform-specific role of Akt in oral cancer. The immunohistochemical analysis of oral cancer tissues showed an overexpression of Akt1 and 2 isoforms but not Akt3. Moreover, the dataset of “The Cancer Genome Atlas” for head and neck cancer has suggested the genetic alterations of Akt1 and 2 tend to be associated with the utmost poor clinical outcome in oral cancer. Further, treatment of oral cancer cells with tobacco and its components such as benzo(a)pyrene and nicotine caused increased mRNA levels of Akt1 and 2 isoforms and also enhanced the aggressiveness of oral cancer cells in terms of proliferation, and clonogenic and migration potential. Finally, silencing of Akt1 and 2 isoforms caused decreased cell survival and induced cell cycle arrest at the G2/M phase. Akt1/2 silencing also reduced tobacco-induced aggressiveness by decreasing the clonogenic and migration potential of oral cancer cells. Moreover, silencing of Akt1 and 2 isoforms was found to decrease the expression of proteins regulating cancer cell survival and proliferation such as cyclooxygenase-2, B-cell lymphoma 2 (Bcl-2), cyclin D1, and survivin. Thus, the important role of Akt1 and 2 isoforms have been elucidated in oral cancer with in-depth mechanistic analysis.

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Section: Discussionsupporting

confidence: 90%

Section: Discussionsupporting

confidence: 62%

Isoform-Specific Role of Akt in Oral Squamous Cell Carcinoma

et al. 2019

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“…In addition, previous studies showed that gallotannin prevented nephrolithiasis via suppression of calcium oxalate crystal binding and oxalate induced oxidative stress in renal epithelial cells 14 . Though gallatonnin showed the proapoptotic actions in colon cancer cells 15 and lung cancer cells A549 16 , underlying anti-cancer mechanism of gallotannin in hepatocellular carcinoma still remains unknown.…”

Section: Introductionmentioning

confidence: 99%

Suppression of E-cadherin Mediates Gallotannin Induced Apoptosis in Hep G2 Hepatocelluar Carcinoma Cells

Han¹,

Kwon²,

Sohn³

et al. 2014

Int. J. Biol. Sci.

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Though gallotannin was known to have anti-oxidant and antitumor activity, the underlying antitumor mechanism of gallotannin still remains unclear. Thus, in the present study, antitumor mechanism of gallotannin was elucidated in hepatocellular carcinoma cells. Gallotannin significantly exerted cytotoxicity against Hep G2 and Chang hepatocellular carcinoma cells with the accumulation of the sub-G1 population and increase of terminal deoxynucleotidyltransferasedUTP nick end labeling (TUNEL) positive cells as an apoptotic feature. Also, gallotannin attenuated the expression of pro-caspase9, pro-caspase3, Bcl2 and integrin β1 and cleaved poly(ADP)-ribose polymerase (PARP) in Hep G2 and Chang cancer cells. Furthermore, gallotannin suppressed cell repair motility by wound healing assay and also inhibited cell adhesion in Hep G2 cells. Of note, gallotannin attenuated the expression of epithelial cadherin (E-cadherin) to form cell-cell adhesion from the early stage, and also beta-catenin at late phase in Hep G2 cells. Consistently, Immunofluorescence assay showed that E-cadherin or β-catenin expression was suppressed in a time dependent manner by gallotannin. Furthermore, silencing of E-cadherin by siRNA transfection method enhanced PAPR cleavage, caspase 3 activation and sub G1 population and attenuated the cell adhesion induced by gallotannin in Hep G2 cells. Overall, our findings demonstrate that the disruption of cell adhesion junction by suppression of E-cadherin mediates gallotannin enhanced apoptosis in Hep G2 liver cancer cells.

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“…In liver cancer HepG2 hepatocellular carcinoma cell line, GT attenuated the expression of pro-caspase9, pro-caspase3, Bcl2, and integrin β1 and cleaved poly(ADP)ribose polymerase [68]. Gallotannin dramatically induced apoptosis through the expression of p53 and active caspase-3 and fragmented DNA in A549 human lung carcinoma cells [69]. In DU145, PC-3, and M2182 prostate cancer cell lines, the inhibition of Mcl-1 and activation of caspases were critically involved in GTinduced apoptosis [70].…”

Section: Gallotannin and Apoptosismentioning

confidence: 95%

Cell Death Mechanisms of the Promising Anticancer Compound Gallotannin

Houssein¹,

Gali‐Muhtasib²

2020

Programmed Cell Death

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The polyphenolic hydrolyzable tannin, gallotannin (GT), also known as tannic acid, possesses interesting anticarcinogenic properties. An evidence from experimental studies suggests that GT is effective against multiple cancer types. Gallotannin has been shown to induce programmed cell death in a wide variety of cancers including colon, breast, prostate, and liver, among others. Apoptosis, cellular senescence, autophagy, and necrosis are the main mechanisms by which GT can suppress cancer progression. In addition, GT is a potent inhibitor of many proliferation pathways. Herein, this chapter provides a summary of our current knowledge about GT's programmed cell death mechanisms against cancer.

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Gallotannin regulates apoptosis and COX-2 expression via Akt and p38kinase pathway in human lung cancer cell line, A549

Cited by 9 publications

References 44 publications

Isoform-Specific Role of Akt in Oral Squamous Cell Carcinoma

Isoform-Specific Role of Akt in Oral Squamous Cell Carcinoma

Suppression of E-cadherin Mediates Gallotannin Induced Apoptosis in Hep G2 Hepatocelluar Carcinoma Cells

Cell Death Mechanisms of the Promising Anticancer Compound Gallotannin

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