Gallic acid, a phenolic acid, hinders the progression of prostate cancer by inhibition of histone deacetylase 1 and 2 expression

Jang, Yin-Gi; Ko, Eul-Bee; Choi, Kyung‐Chul

doi:10.1016/j.jnutbio.2020.108444

Cited by 44 publications

(28 citation statements)

References 62 publications

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“…Since aberrant cell cycle regulation, such as dysregulation of G1/S transition is one of the representative mutations in cancer, cell cycle arrest is considered a potential strategy to eliminate cancer cells (Collins et al, 1997;Evan and Vousden, 2001). Jang et al (2020) revealed that GA induced cell cycle arrest at G2/M phase via up-regulating the expression of p21 and p53 in prostate cancer cells. Therefore, further functional studies related cell cycle are necessary to explain a very faint activation of p21 and p53 by GA compared to CDDP.…”

Section: Discussionmentioning

confidence: 99%

Gallic Acid Hindered Lung Cancer Progression by Inducing Cell Cycle Arrest and Apoptosis in A549 Lung Cancer Cells via PI3K/Akt Pathway

Jang

Kim

et al. 2021

Biomol Ther (Seoul)

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This study elucidates the anti-cancer potential of gallic acid (GA) as a promising therapeutic agent that exerts its effect by regulating the PI3K/Akt pathway. To prove our research rationale, we used diverse experimental methods such as cell viability assay, colony formation assay, tumor spheroid formation assay, cell cycle analysis, TUNEL assay, Western blot analysis, xenograft mouse model and histological analysis. Treatment with GA inhibited cell proliferation in dose-dependent manner as measured by cell viability assay at 48 h. GA and cisplatin (CDDP) also inhibited colony formation and tumor spheroid formation. In addition, GA and CDDP induced apoptosis, as determined by the distribution of early and late apoptotic cells and DNA fragmentation. Western blot analysis revealed that inhibition of the PI3K/Akt pathway induced upregulation of p53 (tumor suppressor protein), which in turn regulated cell cycle related proteins such as p21, p27, Cyclin D1 and E1, and intrinsic apoptotic proteins such as Bax, Bcl-2 and cleaved caspase-3. The anti-cancer effect of GA was further confirmed in an in vivo mouse model. Intraperitoneal injection with GA for 4 weeks in an A549-derived tumor xenograft model reduced the size of tumor mass. Injection of them downregulated the expression of proliferating cell nuclear antigen and p-Akt, but upregulated the expression of cleaved caspase-3 in tumor tissues. Taken together, these results indicated that GA hindered lung cancer progression by inducing cell cycle arrest and apoptosis, suggesting that GA would be a potential therapeutic agent against non-small cell lung cancer.

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Section: Discussionmentioning

confidence: 99%

Gallic Acid Hindered Lung Cancer Progression by Inducing Cell Cycle Arrest and Apoptosis in A549 Lung Cancer Cells via PI3K/Akt Pathway

Jang

Kim

et al. 2021

Biomol Ther (Seoul)

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“…GA is a natural polyphenol with antibacterial, antiviral, and antitumor properties. Its tumor suppressive properties has, thus far, been demonstrated in prostate cancer [ 11 ], breast cancer [ 20 ], bladder cancer [ 21 ], cervical cancer and lung cancer [ 9 ].…”

Section: Discussionmentioning

confidence: 99%

“…Multiple reports have suggested GA to have antibacterial, antiviral, and anti-inflammatory properties. Its anti-tumor activity has been reported in breast [ 8 ], lung [ 9 ], oral [ 10 ], prostate [ 11 ] and cervical cancer cells [ 12 ].…”

Section: Introductionmentioning

confidence: 99%

Gallic Acid Induces S and G2 Phase Arrest and Apoptosis in Human Ovarian Cancer Cells In Vitro

Liu

et al. 2021

Applied Sciences

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Ovarian cancer (OC) is among the top gynecologic cancers in the US with a death tally of 13,940 in the past year alone. Gallic acid (GA) is a natural compound with pharmacological benefits. In this research, the role of GA on cell proliferation, cell apoptosis, cell cycle-related protein expression was explored in OC cell lines OVCAR-3 and A2780/CP70. After 24, 48 and 72 h of GA treatment, the IC50 values in OVCAR-3 cells were 22.14 ± 0.45, 20.36 ± 0.18, 15.13 ± 0.53 μM, respectively and in A2780/CP70 cells IC50 values were 33.53 ± 2.64, 27.18 ± 0.22, 22.81 ± 0.56, respectively. Hoechst 33,342 DNA staining and flow cytometry results showed 20 μM GA exposure could significantly accelerate apoptosis in both OC cell lines and the total apoptotic rate increased from 5.34%(control) to 21.42% in OVCAR-3 cells and from 8.01%(control) to 17.69% in A2780/CP70 cells. Western blot analysis revealed that GA stimulated programmed OC cell death via a p53-dependent intrinsic signaling. In addition, GA arrested cell cycle at the S or G2 phase via p53-p21-Cdc2-cyclin B pathway in the same cells. In conclusion, we provide some evidence of the efficacy of GA in ovarian cancer prevention and therapy.

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“…Similarly, it has been demonstrated that ellagic acid can induce apoptosis in breast, prostrate, colon, and lung cancer cells (Alhakamy et al, 2020, Duan et al, 2020; Mohammed Saleem and Selim, 2020; Yousuf et al, 2020). Gallic acid, another polyphenol present in Triphala preparation also demonstrates significant anticancer and apoptotic activity (Alfei, Marengo, Zuccari, Turrini, & Domenicotti, 2020; Jang, Ko, & Choi, 2020; Patra et al, 2020, Priyadarshi et al, 2020).…”

Section: Discussionmentioning

confidence: 99%

Chebulinic acid inhibits MDA‐MB‐231 breast cancer metastasis and promotes cell death through down regulation of SOD1 and induction of autophagy

Sharma

Mishra

Thacker

et al. 2020

Cell Biology International

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Triple‐negative breast cancers (TNBC) are highly aggressive and drug resistant accounting for majority of cases with poor outcome. Purified natural compounds display substantial anticancer activity with reduced cytotoxicity providing a new avenue to combat TNBC. Chebulinic acid (CA), a polyphenol derived from the fruits of various medicinal plants has potent anticancer activity. Here, we demonstrate that CA shows significant cytotoxicity against triple negative MDA‐MB‐231 cells. CA exhibited cytotoxicity to MDA‐MB‐231 cells in 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide assay. Further, CA mitigated MDA‐MB‐231 cells viability and proliferation as shown by reduced live cell count, crystal violet staining, colony formation assay, soft agar assay and cell cycle analysis. Wound healing assay and trans‐well migration assay demonstrated that CA significantly inhibited migration of MDA‐MB‐231 cells. Also reduced MMP9 expression was observed in CA‐treated cells by gelatin zymography. CA negatively regulated mesenchymal characteristics of MDA‐MB‐231 cells demonstrated by F‐actin staining and reduced expression of N‐cadherin by confocal microscopy and western blot analysis. Annexin V/propidium iodide (PI) and active caspase‐3 staining showed that CA was able to induce apoptosis in MDA‐MB‐231 cells but did not activate caspase‐3. Two‐dimensional gel electrophoresis based proteomic analysis demonstrated that CA regulated proteins belonging to the oxidative stress pathway, apoptotic pathway and proteins with antiproliferative activity. Western blot analysis analysis revealed that CA negatively regulated superoxide dismutase 1 (SOD1) and enhanced oxidative stress in MDA‐MB‐231 cells. SOD1 in‐gel activity assay also showed reduced SOD1 activity upon CA treatment. Overexpression studies with GFP‐LC3 and tandem tagged RFP‐GFP‐LC‐3 also demonstrated enhanced autophagy upon CA treatment.

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Gallic acid, a phenolic acid, hinders the progression of prostate cancer by inhibition of histone deacetylase 1 and 2 expression

Cited by 44 publications

References 62 publications

Gallic Acid Hindered Lung Cancer Progression by Inducing Cell Cycle Arrest and Apoptosis in A549 Lung Cancer Cells via PI3K/Akt Pathway

Gallic Acid Hindered Lung Cancer Progression by Inducing Cell Cycle Arrest and Apoptosis in A549 Lung Cancer Cells via PI3K/Akt Pathway

Gallic Acid Induces S and G2 Phase Arrest and Apoptosis in Human Ovarian Cancer Cells In Vitro

Chebulinic acid inhibits MDA‐MB‐231 breast cancer metastasis and promotes cell death through down regulation of SOD1 and induction of autophagy

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