Bax protein may influence the invasion of colorectal cancer

Pryczynicz, Anna; Gryko, Mariusz; Niewiarowska, Katarzyna; Cepowicz, Dariusz; Ustymowicz, Marek; Kemonä, A; Guzińska‐Ustymowicz, Katarzyna

doi:10.3748/wjg.v20.i5.1305

Cited by 29 publications

(19 citation statements)

References 17 publications

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“…B cell lymphoma (Bcl)-2 homologous antagonist/killer (Bak1) is an essential cell death regulator, which initiates mitochondria-mediated apoptosis by interacting with proteins, including Bcl-extra large (xL) (9) and voltage-dependent anion channels (VDACs) (10). Previous studies have shown that Bcl-2 family proteins, including Bcl-2-associated X protein (Bax), are capable of predicting CRC prognosis, and that Bax agonists efficiently induce apoptosis in tumors (11)(12)(13)(14). However, how their expression is intrinsically controlled in CRC remains to be fully elucidated.…”

Section: Introductionmentioning

confidence: 99%

miR-410 regulates apoptosis by targeting Bak1 in human colorectal cancer cells

Liu

Zhang

Cheng

et al. 2016

Molecular Medicine Reports

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MicroRNAs (miRs) are essential in the pathogenesis of colorectal cancer (CRC). Previous studies have demonstrated that miR‑410 exerts multiple effects on tumors, however, whether it affects the apoptosis of CRC cells remains to be elucidated. In the present study, to demonstrate the role of miR-410 in CRC, miR-410 expression was detected in CRC tissues and cell lines, and the miR-410 level was manipulated by transfection with an miR-410 or miR-410 inhibitor in CRC cells. Cell growth and apoptosis was tested using an MTT assay, western blot and cytochrome C assay. Target validation was conducted by luciferase assay. It was found that miR‑410 was upregulated in CRC tissues and cell lines. The overexpression of miR‑410 resulted in an increase in growth activity and decrease in the extent of apoptosis. By contrast, the inhibition of endogenous miR‑410 activated the apoptotic machinery. Western blot analysis and a luciferase activity assay showed that Bak1 was directly targeted by miR‑410, and that knockdown of Bak1 attenuated the pro‑apoptotic effect of miR‑410 inhibition. In addition, it was shown that the expression of Bak1 was downregulated in CRC tumor tissues and was reversely correlated with the expression of miR‑410, which provided further support that Bak1 was regulated by miR‑410. The results of the present study suggested that miR‑410 may function as an oncogenic miR by suppressing the basal level of apoptosis. These findings may assist in understanding the molecular mechanisms of cancer development.

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Section: Introductionmentioning

confidence: 99%

miR-410 regulates apoptosis by targeting Bak1 in human colorectal cancer cells

Liu

Zhang

Cheng

et al. 2016

Molecular Medicine Reports

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“…The cooperation of KLF4 overexpression and curcumin exhibited a more significant efficiency in inducing the process of apoptosis according to the flow cytometry analysis. Bax and Bcl-2 are the proteins which play important role in cell apoptosis (Theron et al, 2013;Pryczynicz et al, 2014). The further study on evaluating apoptotic proteins levels of BAX and Bcl-2 arrived at the consistent conclusion.…”

Section: Discussionmentioning

confidence: 57%

Synergistic Anti-tumor Effect of KLF4 and Curcumin in Human Gastric Carcinoma Cell Line

Wang²,

Gao³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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“…There is increased Bcl-2 expression in most tumor tissues including breast cancer [10], prostate cancer [11]. On the other hand, in gastric cancer [12] and cutaneous Merkel cell carcinoma [13], Bax expression is obviously increased, while which decrease in colorectal cancer [14] and nasopharyngeal carcinoma [15]. As reported in nonsmall cell lung cancer [16], patients with Bcl-2 overexpression have poor clinical prognosis.…”

Section: Introductionmentioning

confidence: 77%

Gas6/Axl Inhibits Osteosarcoma Apoptosis through Regulation of Apoptosis-Related Protein Bcl-2

Jiang¹,

Lai²

2016

J Bioanal Biomed

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Background: Dysregulation of the receptor tyrosine kinase Axl and its ligand Gas6 has been shown to promote the progression of osteosarcoma and correlates with poor prognosis. This study aimed to identify the role of Gas6/ Axl for anti-apoptosis as induced by cisplatin (DDP) and methotrexate (MTX) chemotherapy and to analyze the relationship between P-Axl and apoptosis-related proteins in osteosarcoma.Method: Cultured osteosarcoma cell lines MG63, 143B and U2OS were used for apoptosis assays, Axl siRNA transfection, cytotoxicity assays, cell cycle analysis, and other assessment methods. A total of 41 cases of osteosarcoma patients were included for immunohistochemistry staining and clinicopathological relative analysis. TUNEL assay was performed in ten pair's cases for apoptosis detection and relative analysis of P-Axl.Results: Among the osteosarcoma cell lines, Gas6 could obviously protect tumor cells from apoptosis induced by DDP and MTX by binding to Axl (P<0.05). Axl siRNA transfection enhanced cell apoptosis, whereas Gas6 was unable to function upon previous knockdown of Axl. Among the 41 osteosarcoma cases, the positive rate of Bcl-2, Bax, and P-Axl was 70.7%, 36.6%, and 85.4%, respectively. In osteofibrous dysplasia, the positive rate of them was 22.2%, 11.1%, and 14.6%, respectively. The expression levels of these apoptosis-related factors were significantly higher in osteosarcoma than in osteofibrous dysplasia (P<0.05). Through clinico-pathological analysis, there were significant relationships between the survival status and Bcl-2 or Bax expression (P<0.05). TUNEL assay also demonstrated that P-Axl high expression inhibited apoptosis in osteosarcoma tissues. By Cox univariate analysis, Bcl-2 or Bax was correlated with the patients' prognosis. Importantly, Pearson correlation analysis demonstrated that Bcl-2 was positively correlated to P-Axl with statistical significance (r=0.842, P<0.0001). Conclusion:Gas6/Axl protects osteosarcoma cells from the apoptosis induced by DDP and MTX chemotherapy and inhibits apoptosis in osteosarcoma tissue, possibly through the regulation of apoptosis-related protein Bcl-2. Bcl-2 was also been proved to be higly expressed in osteosarcoma, but the prognostic or predictive function of Bcl-2 or Bax in osteosarcoma were still uncertain [18], a recent meta-analysis even suggested that the bcl-2 expression might be independent with the prognosis for patients with osteosarcoma [19]. Gas6/Axl InhibitsAs we have proven, osteosarcoma cells show increased levels of activated Axl which are correlated with clinical prognosis. In this setting, Axl protects tumor cells from apoptosis and promotes their invasion and migration, potentially contributing to lung metastasis. Phosphorylated Axl may mediate these effects through Akt signaling and the up regulation of matrix metalloproteinase 9 (MMP-9) [20]. However, studies on the exact inhibition of apoptosis by Axl and the anti-apoptotic mechanisms in osteosarcoma have been rarely reported [21]. ES Papadakis et al. have confirmed th...

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Bax protein may influence the invasion of colorectal cancer

Abstract: Bax protein is probably very significant in the cancerogenesis mechanism in the large intestine.

Cited by 29 publications

References 17 publications

miR-410 regulates apoptosis by targeting Bak1 in human colorectal cancer cells

miR-410 regulates apoptosis by targeting Bak1 in human colorectal cancer cells

Synergistic Anti-tumor Effect of KLF4 and Curcumin in Human Gastric Carcinoma Cell Line

Gas6/Axl Inhibits Osteosarcoma Apoptosis through Regulation of Apoptosis-Related Protein Bcl-2

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