Prognostic Value of Bcl-2 Expression in Squamous Cell Carcinoma of the Larynx: A Systematic Review

Gioacchini, Federico Maria; Alicandri‐Ciufelli, Matteo; Rubini, Corrado; Magliulo, Giuseppe; Re, Massimo

doi:10.5301/jbm.5000116

Cited by 16 publications

(14 citation statements)

References 33 publications

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“…Many studies have demonstrated that cancer stem cells, signal transduction pathways, and hypoxia are vital for the radioresistance of laryngeal carcinoma [26, 41–50]. These roles have also been reported in our previous reviews [25, 51].…”

Section: Radioresistance Of Laryngeal Carcinomasupporting

confidence: 76%

Warburg effect, hexokinase-II, and radioresistance of laryngeal carcinoma

Zhong

Zhou

2016

Oncotarget

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Radiotherapy is now widely used as a part of multidisciplinary treatment approaches for advanced laryngeal carcinoma and preservation of laryngeal function. However, the mechanism of the radioresistance is still unclear. Some studies have revealed that the Warburg effect promotes the radioresistance of various malignant tumors, including laryngeal carcinoma. Among the regulators involved in the Warburg effect, hexokinase-II (HK-II) is a crucial glycolytic enzyme that catalyzes the first essential step of glucose metabolism. HK-II is reportedly highly expressed in some human solid carcinomas by many studies. But for laryngeal carcinoma, there is only one. Till now, no studies have directly targeted inhibited HK-II and enhanced the radiosensitivity of laryngeal carcinoma. Accumulating evidence has shown that dysregulated signaling pathways often result in HK-II overexpression. Here, we summarize recent advances in understanding the association among the Warburg effect, HK-II, and the radioresistance of laryngeal carcinoma. We speculate on the feasibility of enhancing radiosensitivity by targeted inhibiting HK-II signaling pathways in laryngeal carcinoma, which may provide a novel anticancer therapy.

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Section: Radioresistance Of Laryngeal Carcinomasupporting

confidence: 76%

Warburg effect, hexokinase-II, and radioresistance of laryngeal carcinoma

Zhong

Zhou

2016

Oncotarget

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“…The study was limited by the absence of a control group receiving no neoadjuvant chemotherapy. Studies evaluating the prognostic value of Bcl-2 have reported conflicting results [25]. Although one study found that a high level of Bcl-2 protein was associated with a poorer response to different treatment modalities in different cancer types [26], the opposing view was also supported by studies correlating Bcl-2 positivity with improved prognosis [12,14].…”

Section: Discussionmentioning

confidence: 99%

Is Bcl-2 a predictive marker of neoadjuvant chemotherapy response in patients with urothelial bladder cancer undergoing radical cystectomy?

Türker

Segersten

Malmström

et al. 2019

Scandinavian Journal of Urology

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Background: Response to neoadjuvant cisplatin treatment in bladder cancer has been linked to expression of Bcl-2 protein by cancer cells. The objective of this study was to test Bcl-2 as a predictive marker of neoadjuvant cisplatin chemotherapy response in a patient cohort from randomized cystectomy trials. Methods: Tumor samples were taken from 247 patients with T2-T4 bladder cancer enrolled in two randomized trials comparing cystectomy with or without neoadjuvant chemotherapy. Tissue microarrays from pre-intervention transurethral resection specimens were assessed for Bcl-2 protein status by immunohistochemistry. Extension of staining above 10% was regarded as positive. Downstaging and survival ratios in relation to Bcl-2 immunoreactivity and neoadjuvant chemotherapy utilization were calculated using the log rank test and multivariate Cox proportional hazards regression analyses. Results: Bcl-2 expression was positive in 38% and negative in 62% of the 236 evaluable patients. Bcl-2 negative patients receiving neoadjuvant chemotherapy had a significant increase in survival (p ¼ 0.009), while Bcl-2 positive patients showed no difference (p ¼ 0.4). However, the interaction variable between neoadjuvant chemotherapy and biomarker status was not significant (p ¼ 0.38). When the prognostic value was assessed in the no-chemotherapy group, 5-year overall survival times were significantly better among Bcl-2 positive patients than among Bcl-2 negative patients (42 months vs 33 months, p ¼ 0.04), but again Bcl-2 status did not remain independent when other factors were adjusted. Also, in a multivariate analysis with all patients, Bcl-2 was not significant. Conclusions: Bcl-2 status is not an independent predictor of neoadjuvant cisplatin chemotherapy response and is not prognostic in muscle-invasive bladder cancer.

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“…Apoptosis is the only way to renew cells. Apoptosis of endothelial cells after ischemia reperfusion injury may be due to the severe downregulation of anti-apoptotic factor Bcl-2 ( 13 , 14 ). In that study through the in vitro culture of CMVEC cells PGA1 and TRI intervention therapy was administered, suggesting that PGA1 and TRI significantly improved the decreased expression of Bcl-2 mRNA induced by myocardial ischemia reperfusion.…”

Section: Discussionmentioning

confidence: 99%

Inhibitory effects of PGA1 and TRI on the apoptosis of cardiac microvascular endothelial cells of rats

et al. 2017

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The present study investigated the protective effects and molecular mechanism of prostaglandin A1 (PGA1) and triptolide (TRI) on apoptosis of cardiac microvascular endothelial cells (CMVECs) in rats. CMVECs of rats were isolated and then cultured. MTT method was used to select and establish a cell hypoxia reoxygenation cell model. The cells were divided into four groups: Normoxia control group (C, normal oxygen), hypoxia reoxygenation group (H/R, hypoxia for 12 h/reoxygenation for 6 h), PGA1 group (H/R+PGA1) and TRI group (H/R+TRI). The growth of cells in each of the group was observed. B-cell lymphoma 2 (Bcl-2) mRNA expression in CMVECs and expression of Bcl-2 mRNA after PGA1 and TRI treatment were determined by RT-PCR. Cell apoptosis was detected by terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) assay. Bcl-2 mRNA decreased significantly after hypoxia stimulation of CMVECs of rats. The expression of Bcl-2 mRNA was significantly higher in comparison to hypoxia stimulation group after treatment with PGA1 and TRI (P<0.01). The elevated effect of PGA1 on Bcl-2 mRNA was stronger than that of the TRI group (P<0.05). The number of CMVECs reduced significantly after hypoxia. By contrast, DNA fragmentation and the number of endothelial cell apoptosis were increased significantly. However, Bcl-2 mRNA expression decreased significantly, after PGA1 and TRI treatments. Furthermore, the number of apoptotic cells reduced and Bcl-2 mRNA expression increased (P<0.01). PGA1 and TRI significantly upregulated the expression of Bcl-2 mRNA, inhibited the activation of CMVECs and were able to achieve the protective effect on apoptosis of CMVECs in hypoxia-oxygenated rats.

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Prognostic Value of Bcl-2 Expression in Squamous Cell Carcinoma of the Larynx: A Systematic Review

Cited by 16 publications

References 33 publications

Warburg effect, hexokinase-II, and radioresistance of laryngeal carcinoma

Warburg effect, hexokinase-II, and radioresistance of laryngeal carcinoma

Is Bcl-2 a predictive marker of neoadjuvant chemotherapy response in patients with urothelial bladder cancer undergoing radical cystectomy?

Inhibitory effects of PGA1 and TRI on the apoptosis of cardiac microvascular endothelial cells of rats

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