Cell survival and apoptosis‐related molecules in cancer cells in effusions: A comprehensive review

Kleinberg, Lilach; Davidson, Ben

doi:10.1002/dc.21095

Cited by 16 publications

(10 citation statements)

References 165 publications

(160 reference statements)

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“…The inhibition of NF-κB by NO donors was found to lead to the repression of anti-apoptotic target genes including YY1 , further illustrating YY1 as a direct target gene of NF-κB. 10,13 Likewise, reports by Karin et al, 36 Hongo et al, 37 and Kleinberg et al 38 further corroborated that NF-κB regulates the activation of YY1 and also other genes such as the X-linked inhibitor of apoptosis protein (XIAP) and the B-cell lymphoma-extra large (Bcl-xL) through direct targeting.…”

Section: Indirect Regulation Of Emt By Yy1 Through the Nf-κb/snamentioning

confidence: 88%

Targeting the Overexpressed YY1 in Cancer Inhibits EMT and Metastasis

Cho

Bonavida

2017

Crit Rev Oncog

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There have been recent developments in the treatment of various cancers, in particular non-metastatic cancers. However, many of the responding patients often relapse initially through the development of spread micro-and macro-metastases. Unfortunately, there are very few therapeutic modalities for the treatment of metastatic cancers. The development of cancer metastasis has been proposed to involve the epithelial–mesenchymal transition (EMT), in which the tumor cells with the EMT phenotype exhibit various phenotypic markers and molecular modifications that are manifested to resist most conventional therapies. YY1 is a target of the hyperactivated nuclear factor-kappa beta pathway in cancer and it was reported that YY1 also regulates cell survival and cell proliferation in addition to its role in EMT and resistance. The overexpression of YY1 in the majority of cancers has been correlated with poor prognosis. It is hypothesized that targeting YY1 may result in several anti-tumor activities, including inhibition of cell survival and cell proliferation, inhibition of EMT, and reversal of resistance. This review discusses the potential therapeutic targeting of an overexpressed transcription factor, Yin Yang 1 (YY1), which has been implicated in the development of EMT and drug resistance. Several examples targeting YY1 in experimental models are presented.

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Section: Indirect Regulation Of Emt By Yy1 Through the Nf-κb/snamentioning

confidence: 88%

Targeting the Overexpressed YY1 in Cancer Inhibits EMT and Metastasis

Cho

Bonavida

2017

Crit Rev Oncog

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“…in accordance with the results for Bax/Bcl-2, HSP47 overexpression also resulted in increased expression of cleaved caspase-7/-8/-9 and PARP. Caspase-8 and caspase-9 both play a role in the extrinsic apoptotic pathway and the intrinsic mitochondrial apoptotic pathway, respectively, given that both of them can activate downstream caspase family proteins, such as caspase-7 (44,49,50). Therefore, it appears that HSP47 induces apoptosis via both the extrinsic and the intrinsic mitochondrial apoptosis pathways.…”

Section: Discussionmentioning

confidence: 99%

HSP47 is associated with the prognosis of laryngeal squamous cell carcinoma by inhibiting cell viability and invasion and promoting apoptosis

et al. 2017

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Abstract. Heat shock protein 47 (HSP47) is a 47 kDa collagen binding protein that has a close relationship with the development and progression of tumours. However, little is known concerning the expression profile of HSP47 in laryngeal squamous cell carcinoma (LSCC) patients and there is still insufficient data concerning the underlying mechanisms. The aim of the present study was to explore the expression of HSP47 in LSCC and provide an overview of its association with tumourigenicity and clinical prognosis. The expression of HSP47 in LSCC and adjacent non-cancerous laryngeal tissues was assessed via western blotting and immunohistochemical studies. The prognostic significance of HSP47 expression was analysed using a Kaplan-Meier survival curve. To investigate the influence of HSP47 on the viability, invasion and apoptosis of a LSCC cell line, we performed an in vitro analysis with plasmid vectors and small interfering RNA (siRNA). Our results showed that HSP47 protein expression in the LSCC tissues was markedly decreased compared to that noted in the adjacent non-cancerous tissues, and low expression of HSP47 was correlated with poor prognosis in LSCC patients. Upregulation of HSP47 via plasmid vectors inhibited the proliferation, reduced the invasive ability, increased the sensitivity to cisplatin chemotherapy, promoted apoptosis, and induced the G1 phase arrest of LSCC cells in vitro. The expression of apoptosis-regulating proteins was also altered when HSP47 was upregulated, involving increased expression of cleaved caspase-7/-8/-9, PARP, and Bax and decreased expression of Bcl-2. Our present data suggest that HSP47 is an important prognostic factor and an attractive therapeutic target in LSCC due to its influence on the biological behaviour of LSCC cells.

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“…The intrinsic pathway releases cytochrome c to form apoptosome to activate caspase 9/3 in the cells (Ouyang et al, ), whereas extrinsic pathway is triggered by binding of Fas and plasma membrane death receptor with its extracellular ligand Fas‐L to activate caspase 8/3. Thus, recently, apoptosis is an important target for cancer therapy (Kleinberg and Davidson, ; Ouyang et al, ). In the current study, GBA showed cytotoxicity in wild EGFR type H460 and A549 cells better than other mutant type PC‐9 and HCC827 NSCLC cells, implying EGFR may mediate the cytotoxicity of GBA in wild EGFR type H460 and A549 cells.…”

Section: Discussionmentioning

confidence: 99%

Apoptotic Effect of Galbanic Acid via Activation of Caspases and Inhibition of Mcl‐1 in H460 Non‐Small Lung Carcinoma Cells

Shin

Jung

et al. 2015

Phytotherapy Research

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Galbanic acid (GBA), a major compound of Ferula assafoetida, was known to have cytotoxic, anti-angiogenic and apoptotic effects in prostate cancer and murine Lewis lung cancer cells; the underling apoptotic mechanism of GBA still remains unclear so far. Thus, in the present study, the apoptotic mechanism of GBA was investigated mainly in H460 non-small cell lung carcinoma (NSCLC) cells because H460 cells were most susceptible to GBA than A549, PC-9 and HCC827 NSCLC cells. Galbanic acid showed cytotoxicity in wild EGFR type H460 and A549 cells better than other mutant type PC-9 and HCC827 NSCLC cells. Also, GBA significantly increased the number of Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) positive cells and sub G1 population in H460 cells. Western blotting revealed that GBA cleaved poly (ADP-ribose) polymerase (PARP), activated Bax and caspase 9, attenuated the expression of Bcl-2, Bcl-x(L), and Myeloid cell leukemia 1 (Mcl-1) in H460 cells. However, interestingly, overexpression of Mcl-1 blocked the ability of GBA to exert cytotoxicity, activate caspase9 and Bax, cleave PARP, and increase sub G1 accumulation in H460 cells. Overall, these findings suggest that GBA induces apoptosis in H460 cells via caspase activation and Mcl-1 inhibition in H460 cells as a potent anticancer agent for NSCLC treatment.

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Cell survival and apoptosis‐related molecules in cancer cells in effusions: A comprehensive review

Cited by 16 publications

References 165 publications

Targeting the Overexpressed YY1 in Cancer Inhibits EMT and Metastasis

Targeting the Overexpressed YY1 in Cancer Inhibits EMT and Metastasis

HSP47 is associated with the prognosis of laryngeal squamous cell carcinoma by inhibiting cell viability and invasion and promoting apoptosis

Apoptotic Effect of Galbanic Acid via Activation of Caspases and Inhibition of Mcl‐1 in H460 Non‐Small Lung Carcinoma Cells

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