Upregulation of Mcl-1 inhibits JQ1-triggered anticancer activity in hepatocellular carcinoma cells

Zhang, Huapeng; Li, Gong-Quan; Zhang, Yi; Guo, Wenzhi; Zhang, Jiakai; Li, Jie; Lv, Jianfeng; Zhang, Shuijun

doi:10.1016/j.bbrc.2017.12.153

Cited by 16 publications

(10 citation statements)

References 18 publications

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“…Both Mcl-1 and Bim are two critical proteins involved in regulation of the intrinsic apoptotic pathway (41)(42)(43). While some studies have shown that BET inhibitors such as JQ1 increased Bim expression in some cancer cells (44)(45)(46), one study reported that JQ-1 even increased Mcl-1 expression (47). A recent study showed that the BET degrader, BETd-246 (ZBC-246), an analogue of ZBC260, decreased Mcl-1 levels in breast cancer cells, which contributes to the induction of apoptosis by BETd-246 (12).…”

Section: Discussionmentioning

confidence: 99%

BRD4 Levels Determine the Response of Human Lung Cancer Cells to BET Degraders That Potently Induce Apoptosis through Suppression of Mcl-1

Cavalcante

Yao

et al. 2020

Cancer Research

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Section: Discussionmentioning

confidence: 99%

BRD4 Levels Determine the Response of Human Lung Cancer Cells to BET Degraders That Potently Induce Apoptosis through Suppression of Mcl-1

Cavalcante

Yao

et al. 2020

Cancer Research

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“…Generally, flavopiridol initiates cell cycle arrest and apoptosis in a p53-independent mechanism that involves the down regulation of anti-apoptotic Mcl-1 and x-IAP and induction of ER stress [168,169,170,171]. In HCC the inhibitory effect of flavopiridol was associated with Mcl-1 inhibition that enhanced caspase-3 activation and PARP cleavage [172]. Interestingly, doxorubicin applied in combination with flavopiridol in HCC mouse models significantly reduced proliferative signaling [173].…”

Section: Phytochemicalsmentioning

confidence: 99%

Flavonoids in Cancer and Apoptosis

Abotaleb

Samuel

Varghese

et al. 2018

Cancers

539

394

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Cancer is the second leading cause of death globally. Although, there are many different approaches to cancer treatment, they are often painful due to adverse side effects and are sometimes ineffective due to increasing resistance to classical anti-cancer drugs or radiation therapy. Targeting delayed/inhibited apoptosis is a major approach in cancer treatment and a highly active area of research. Plant derived natural compounds are of major interest due to their high bioavailability, safety, minimal side effects and, most importantly, cost effectiveness. Flavonoids have gained importance as anti-cancer agents and have shown great potential as cytotoxic anti-cancer agents promoting apoptosis in cancer cells. In this review, a summary of flavonoids and their effectiveness in cancer treatment targeting apoptosis has been discussed.

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“…Next, NRK-52E cells were transfected with small interfering RNA (siRNA) negative control (NC) in one group and with caspase-11 siRNA in another. Then, the cells in both groups were subjected to hypoxic conditions for 3 h, and reoxygenation for 6 h. Finally, we harvested the cells, extracted RNA, reverse transcribed RNA into cDNA, and extracted cell proteins as previously described [19]. Transfection effects of siRNA were determined by RT-qPCR and western blotting.…”

Section: Animal Groups and Treatmentmentioning

confidence: 99%

Caspase-1 Inhibitor Reduces Pyroptosis in Kidney Injury Induced by Brain Death

Liu¹,

Yang²,

Shi³

et al. 2021

Preprint

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Brain death (BD) induces an organ-level inflammatory response, and BD donor kidneys show inferior survival and recovery rates. However, the underlying mechanisms have not been fully elucidated. Here, we investigated the role of caspase-1-mediated pyroptosis in BD-induced kidney injury in rats. A BD model was established in Sprague-Dawley rats. The rats were intravenously injected with a caspase-1 inhibitor (Z-YVAD-FMK) 1 h before BD, and sham-operated rats served as controls. After 0, 1, 2, 4, and 6 h of BD, renal function, renal injury, and renal expression of NLRP3, caspase-1, caspase-11, gasdermin D (GSDMD), IL-1β, and IL-18 were assessed using quantitative reverse transcriptase-polymerase chain reaction, western blotting, and immunohistochemistry. Blood urea nitrogen and serum creatinine levels were measured. Additionally, renal tubular epithelial cells (NRK-52E) were subjected to 3 h of hypoxia followed by 6 h of reoxygenation and incubated with Z-YVAD-FMK before hypoxia and reoxygenation. Caspase-11 was knocked-down using small interfering RNA technology. Cell viability and levels of pyroptosis-associated proteins were assessed thereafter. NLRP3, caspase-1, GSDMD, IL-1β, and IL-18 expression levels were upregulated in BD rats. Treatment with Z-YVAD-FMK reduced mRNA and protein levels, improved renal function, and alleviated renal injury. Z-YVAD-FMK effectively reduced pyroptosis in BD rats; however, it did not affect caspase-11 expression in vivo or in vitro. Thus, it could be considered as a therapeutic target for BD-induced kidney injury.

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Upregulation of Mcl-1 inhibits JQ1-triggered anticancer activity in hepatocellular carcinoma cells

Cited by 16 publications

References 18 publications

BRD4 Levels Determine the Response of Human Lung Cancer Cells to BET Degraders That Potently Induce Apoptosis through Suppression of Mcl-1

BRD4 Levels Determine the Response of Human Lung Cancer Cells to BET Degraders That Potently Induce Apoptosis through Suppression of Mcl-1

Flavonoids in Cancer and Apoptosis

Caspase-1 Inhibitor Reduces Pyroptosis in Kidney Injury Induced by Brain Death

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