Expression of Caspase-1 in breast cancer tissues and its effects on cell proliferation, apoptosis and invasion

Sun, Yanxia; Guo, Yingzhen

doi:10.3892/ol.2018.8176

Cited by 19 publications

(17 citation statements)

References 25 publications

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“…Notably, previous studies have indicated that caspase-1 activation and IL-1β secretion contribute to pyroptotic cell death in estrogen receptor (ER)-negative breast cancer cells [27,44], which are contrary to our present observations in ER-positive breast cancer cells. Indeed, the tumor growth suppressing effect of inflammasomes inhibitors was not detected in triple-negative MDA-MB-231 cells in our study ( Figure S2B), suggesting a possibility that ERα signaling plays a role in the linkage between inflammasomes and breast tumor growth.…”

Section: Discussioncontrasting

confidence: 99%

“…Although MCC950, a potent small molecule inhibitor of NLRP3 inflammasome, was previously reported to inhibit survival, migration, and invasion in head, neck, and lung cancer [42,43], the effect of caspase-1 inhibitors, such as Ac-YVAD-cmk, on tumor growth remains controversial. In a study performed by Sun et al, treatment with Ac-YVAD-cmk markedly increased cell proliferation and invasion, and decreased apoptotic levels in MDA-MB-231 breast cancer cells [44]. By contrast, the inhibition of caspase-1 by Ac-YVAD-CHO led to apoptosis in pancreatic carcinoma cells [45], implying that the role of caspase-1 in the survival and growth of cancer cells is also depending on the experimental condition, particularly determined by cancer cell types.…”

Section: Discussionmentioning

confidence: 96%

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Globular Adiponectin Inhibits Breast Cancer Cell Growth through Modulation of Inflammasome Activation: Critical Role of Sestrin2 and AMPK Signaling

Pham

Raut

Pandit

et al. 2020

Cancers

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Adiponectin, an adipokine predominantly derived from adipose tissue, exhibits potent antitumor properties in breast cancer cells. However, its mechanisms of action remain elusive. Inflammasomes—intracellular multimeric protein complexes—modulate cancer cell growth in a complicated manner, as well as playing a role in the innate immune system. Herein, we examined the potential role of inflammasomes in the antitumor activity of adiponectin and found that globular adiponectin (gAcrp) significantly suppressed inflammasomes activation in breast cancer cells both in vitro and in vivo conditions, as determined by decreased expression of inflammasomes components, including NOD-like receptor pyrin domain-containing protein 3 (NLRP3) and the apoptosis-associated speck-like protein containing a CARD (ASC), and inhibition of interleukin-1β and caspase-1 activation. Treatment with pharmacological inhibitors of inflammasomes caused decrease in cell viability, apoptosis induction, and G0/G1 cell cycle arrest, suggesting that inflammasomes activation is implicated in the growth of breast cancer cells. In addition, treatment with gAcrp generated essentially similar results to those of inflammasomes inhibitors, further indicating that suppression of breast cancer cell growth by gAcrp is mediated via modulation of inflammasomes. Mechanistically, gAcrp suppressed inflammasomes activation through sestrin2 (SESN2) induction, liver kinase B1 (LKB-1)-dependent AMP-activated protein kinase (AMPK) phosphorylation, and alleviation of endoplasmic reticulum (ER) stress. Taken together, these results demonstrate that gAcrp inhibits growth of breast cancer cells by suppressing inflammasomes activation, at least in part, via SESN2 induction and AMPK activation-dependent mechanisms.

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Section: Discussioncontrasting

confidence: 99%

Section: Discussionmentioning

confidence: 96%

Globular Adiponectin Inhibits Breast Cancer Cell Growth through Modulation of Inflammasome Activation: Critical Role of Sestrin2 and AMPK Signaling

Pham

Raut

Pandit

et al. 2020

Cancers

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“…Upregulation of this gene and NF‐κB/RELA signaling is observed following androgen stimulation of androgen‐dependent LNCaP cells 18 . However, contradictory to our findings of CASP‐1 overexpression, downregulation of caspase‐1 is observed in breast cancer, and when knocked out provided a highly proliferative environment for colon epithelial cells and the development of colon tumors 32‐34 . Interestingly, when we analyzed only those patients who were diagnosed with CaP, all DE genes in cancer class 1 were also DE in all samples in class 1 including EGRF , AKT1 , CASP‐1 , and NFκB .…”

Section: Discussioncontrasting

confidence: 77%

Inflammatory infiltration is associated with AR expression and poor prognosis in hormone naïve prostate cancer

et al. 2020

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Background Tumor microenvironment inflammatory infiltration is proposed as a protumorigenic mechanism for prostate cancer with proinflammatory cytokines stimulating androgen receptor (AR) activity. However, association with patient prognosis remains unclear. This study derives an inflammatory gene signature associated with AR expression and investigates CD3+ and CD8+ T‐lymphocyte infiltration association with AR and prognosis. Methods Gene profiling of inflammatory related genes was performed on 71 prostate biopsies. Immunohistochemistry on 243 hormone‐naïve prostate cancers was performed for CD3, CD8, AR, and phosphorylated AR tumor expression. Results Multiple proinflammatory genes were differentially expressed in association with high AR expression compared with low AR expression including PI3KCA and MAKP8 (adjusted P < .05). High CD3+ and high CD8+ infiltration associated with reduced cancer‐specific survival (P = .018 and P = .020, respectively). High CD3+ infiltration correlated with high tumor cytoplasmic AR expression and if assessed together, they associated with reduced cancer‐specific and 5‐year survival from 90% to 56% (P = .000179). High CD8+ cytotoxic infiltration associated with high androgen‐independent tumor nuclear AR serine 213 phosphorylation (correlation coefficient = 0.227; P = .003) and when assessed together associated with poor clinico‐pathological features including perineural invasion (P = .001). Multiple genes involved in proinflammatory signaling pathways are upregulated in high AR expressing prostate samples. Conclusion T‐lymphocyte infiltration in hormone‐naïve disease associates with androgen‐independent driven disease and provides possible therapeutic targets to reduce transformation from hormone‐naïve to castrate‐resistant disease.

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“…ARRDC3 has been reported to suppress breast carcinoma invasion (68). The downregulation of the expression of CASP1 has been shown to result in the proliferation and invasion of breast cancer cells (69). In this study, the functions of SEMA5A were further validated in in vitro (Fig.…”

Section: Discussionmentioning

confidence: 99%

Semaphorin 5A suppresses the proliferation and migration of lung adenocarcinoma cells

Lenka

Yuan

et al. 2019

Int J Oncol

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Semaphorin 5A (SEMA5A), a member of the semaphorin family, plays an important role in axonal guidance. Previously, the authors identified another possible role of SEMA5A as a prognostic biomarker for non-smoking women with lung adenocarcinoma in Taiwan, and this phenomenon has been validated in other ethnic groups. However, the functional significance of SEMA5A in lung adenocarcinoma remains unclear. Therefore, we assessed the function of SEMA5A in three lung adenocarcinoma cell lines in this study. Kaplan-Meier Plotter for lung cancer was conducted for survival analyses. Reverse transcription-quantitative PCR (RT-qPCR) and western blot analysis were performed to investigate the expression and post-translational regulation of SEMA5A in lung adenocar-cinoma cell lines. A pre-designed PyroMark CpG assay and 5-aza-2′-deoxycytidine treatment were used to measure the methylation levels of SEMA5A. The biological functions of lung adenocarcinoma cells overexpressing SEMA5A were investigated by microarrays, and validated both in vitro (proliferation, colony formation and migration assays) and in vivo (tumor xenografts) experiments. The results revealed that the hypermethylation of SEMA5A and the cleavage of the extracellular domain of SEMA5A were responsible for the downregulation of the SEMA5A levels in lung adenocarcinoma cells (A549 and H1299) as compared to the normal controls. Functional analysis of SEMA5A-regulated genes revealed that they were involved in cellular growth and proliferation. The overexpression of SEMA5A in A549 and H1299 cells significantly decreased the proliferation (P<0.01), colony formation (P<0.001) and migratory ability (P<0.01) of the cells. The suppressive effects of SEMA5A on the proliferative and migratory ability of the cells were also observed in both in vitro and in vivo experiments using brain metastatic Bm7 lung adenocarcinoma cells. On the whole, the findings of this study suggest a suppressive role for SEMA5A in lung adenocarcinoma involving the inhibition of the proliferation and migration of lung transformed cells.

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Expression of Caspase-1 in breast cancer tissues and its effects on cell proliferation, apoptosis and invasion

Cited by 19 publications

References 25 publications

Globular Adiponectin Inhibits Breast Cancer Cell Growth through Modulation of Inflammasome Activation: Critical Role of Sestrin2 and AMPK Signaling

Globular Adiponectin Inhibits Breast Cancer Cell Growth through Modulation of Inflammasome Activation: Critical Role of Sestrin2 and AMPK Signaling

Inflammatory infiltration is associated with AR expression and poor prognosis in hormone naïve prostate cancer

Semaphorin 5A suppresses the proliferation and migration of lung adenocarcinoma cells

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