Apoptotic effect of resveratrol on human T‐ALL cell line CCRF‐CEM is unlikely exerted through alteration of <i>BAX</i> and <i>BCL2</i> promoter methylation

Heydarabad, Milad Zadi; Vatanmakanian, Mousa; Abdolalizadeh, Jalal; Mohammadi, Hamed; Azimi, Ako; Ardehaie, Reza Mousavi; Movasaghpour, Aliakbar

doi:10.1002/jcb.27333

Cited by 9 publications

(6 citation statements)

References 28 publications

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“…The BAG family was first identified as a group of proteins that prevent cell death through their interaction with Bcl-2 (20). The Bcl-2 family genes (Bcl-2 and Bax) play critical roles in the apoptosis of T-ALL cells (41,42). In the present study, the results also demonstrated that the protein expression levels of Bcl-2 were decreased and the levels of Bax were increased simultaneously following the downregulation of the levels of BAG2.…”

Section: Discussionsupporting

confidence: 68%

MicroRNA‑325 inhibits the proliferation and induces the apoptosis of T cell acute lymphoblastic leukemia cells in a BAG2‑dependent manner

Wang

Zhang

et al. 2021

Exp Ther Med

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The inhibitory effect of microRNA (miR)-325 in multiple different types of cancer cell has been identified; however, its biological function in T cell acute lymphoblastic leukemia (T-ALL) remains unknown. Moreover, Bcl-2-associated athanogene (BAG)2 is highly expressed in a various types of tumors and is regarded as an anti-apoptotic gene. In the present study, the roles of miR-325 and BAG2 in a T-ALL cell line (Jurkat cells) were investigated. BAG2 and miR-325 expression levels in clinical blood samples from healthy donors and pediatric patients with T-ALL, as well as in T-ALL cell lines was detected using western blot analysis and/or reverse transcription-quantitative PCR. Dual-luciferase reporter gene assays and TargetScan were used to evaluate the interaction between BAG2 and miR-325. Small interfering RNA technology was applied to knockdown BAG2 expression in Jurkat cells. The effects of miR-325 mimic and BAG2 downregulation on the proliferation and apoptosis were assessed by an MTT assay, flow cytometry and western blot analysis. The results revealed that the expression of miR-325 was downregulated in blood samples from pediatric patients and in T-ALL cell lines, and its expression was lowest in Jurkat cells. The expression levels of BAG2 exhibited the opposite results. The knockdown of BAG2 markedly induced the apoptosis and inhibited the proliferation of Jurkat cells. In addition, the overexpression of miR-325 significantly inhibited the growth and promoted the apoptosis of Jurkat cells, with these effects being eliminated by BAG2 overexpression. In conclusion, the findings of the present study demonstrated that miR-325 directly targets the BAG2 gene and that the introduction of miR-325 can accelerate apoptosis and suppress the proliferation of Jurkat cells by silencing BAG2 expression.

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Section: Discussionsupporting

confidence: 68%

MicroRNA‑325 inhibits the proliferation and induces the apoptosis of T cell acute lymphoblastic leukemia cells in a BAG2‑dependent manner

Wang

Zhang

et al. 2021

Exp Ther Med

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“…Zadi Heydarabad and colleagues showed that DNA methylation of BAX and BCL2 genes in a T-cell acute lymphoblastic leukemia cell line, CCRF-CEM, can be detected after resveratrol treatment by a methylation-specific polymerase chain reaction technique. They suggested that this observation might explain the effect of resveratrol in sensitizing ALL cells to apoptosis [ 131 ]. In another study, the effect of resveratrol on retinoic acid resistance in the anaplastic thyroid cancer cell line THJ-11T and the human medulloblastoma UW228-2 cell line showed that resveratrol not only demethylates the cellular retinoic acid binding protein 2 (CRABP2) promotor but also decreases the amounts of some DNA methyltransferases such as DNMT1, 3A, and 3B [ 132 ].…”

Section: Polyphenols Modulate Cancer Drug Resistancementioning

confidence: 99%

The role of polyphenols in overcoming cancer drug resistance: a comprehensive review

et al. 2022

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Chemotherapeutic drugs are used to treat advanced stages of cancer or following surgery. However, cancers often develop resistance against drugs, leading to failure of treatment and recurrence of the disease. Polyphenols are a family of organic compounds with more than 10,000 members which have a three-membered flavan ring system in common. These natural compounds are known for their beneficial properties, such as free radical scavenging, decreasing oxidative stress, and modulating inflammation. Herein, we discuss the role of polyphenols (mainly curcumin, resveratrol, and epigallocatechin gallate [EGCG]) in different aspects of cancer drug resistance. Increasing drug uptake by tumor cells, decreasing drug metabolism by enzymes (e.g. cytochromes and glutathione-S-transferases), and reducing drug efflux are some of the mechanisms by which polyphenols increase the sensitivity of cancer cells to chemotherapeutic agents. Polyphenols also affect other targets for overcoming chemoresistance in cancer cells, including cell death (i.e. autophagy and apoptosis), EMT, ROS, DNA repair processes, cancer stem cells, and epigenetics (e.g. miRNAs).

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“…Resveratrol is a natural polyphenol compound with a variety of biological activities, such as antioxidant, anti-inflammatory, immunoregulatory, chemopreventive and antitumor activities (19). Resveratrol treatment has been shown to trigger the apoptosis of the T-acute lymphoblastic leukemia (T-ALL) cell line, ccRF-cEM, via the upregulation of the apoptotic BAX gene and the downregulation of the anti-apoptotic BcL2 gene (20). Apoptosis has also been shown to be induced in TRAIL-resistant lung cancer cells following co-treatment with resveratrol and TRAIL via the suppression of Akt/NF-κB signaling (21).…”

Section: Resveratrol Inhibits the Progression Of Cervical Cancer By Smentioning

confidence: 99%

Resveratrol inhibits the progression of cervical cancer by suppressing the transcription and expression of HPV E6 and E7 genes

Sun

Xie

et al. 2020

Int J Mol Med

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Resveratrol is a representative polyphenol of diet-derived putative cancer chemopreventive agents, which have attracted increasing interest in the cancer chemoprevention community. The inhibition of the action of human papillomavirus (HPV) E6 and E7 has been considered a key approach for cervical cancer therapy. Resveratrol has been shown to induce the apoptosis, and reduce both the viability and mitotic index of a number of cancer cell lines, including human cervical cancer cells. In the present study, it was confirmed that resveratrol inhibited the HPV E6 mRNA, HPV E6 protein and phosphorylated retinoblastoma protein (p-pRb1) levels, and increased the p53 protein levels in HeLa and Ca Ski cells, as well as in subcutaneous tumor tissue grown from HeLa cells. High-risk HPV uses a bicistronic RNA to control E6 and E7 genes simultaneously. On the whole, the present study demonstrates that resveratrol inhibits cervical cancer development by suppressing the transcription and translation of E6 and E7, and also by promoting the apoptosis and G1/S phase transition arrest. These findings may provide the basis for the development of resveratrol as a candidate for cervical cancer therapy.

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Apoptotic effect of resveratrol on human T‐ALL cell line CCRF‐CEM is unlikely exerted through alteration of BAX and BCL2 promoter methylation

Cited by 9 publications

References 28 publications

MicroRNA‑325 inhibits the proliferation and induces the apoptosis of T cell acute lymphoblastic leukemia cells in a BAG2‑dependent manner

MicroRNA‑325 inhibits the proliferation and induces the apoptosis of T cell acute lymphoblastic leukemia cells in a BAG2‑dependent manner

The role of polyphenols in overcoming cancer drug resistance: a comprehensive review

Resveratrol inhibits the progression of cervical cancer by suppressing the transcription and expression of HPV E6 and E7 genes

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