The anti-apoptotic effect of regucalcin is mediated through multisignaling pathways

Yamaguchi, Masayoshi

doi:10.1007/s10495-013-0859-x

Cited by 76 publications

(79 citation statements)

References 63 publications

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“…Apoptosis is considered to be promoted in cells with high Bax protein expression and inhibited in cells with high Bcl-2 protein expression. Several previous studies have also confirmed the role of both proteins in lung cancer cells (43)(44)(45). The current results suggest that in A549/DDP cells, I 131 and GA alone are able to regulate the protein expression levels of Bcl-2 and Bax.…”

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confidence: 86%

Role of gambogic acid and NaI131 in A549/DDP cells

et al. 2016

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Abstract. Resistance to platinum in tumor tissue is a considerable barrier against effective lung cancer treatment. Radionuclide therapy is the primary adjuvant treatment, however, the toxic side effects limit its dosage in the clinical setting. Therefore, the present study aimed to determine whether an NaI 131 radiosensitizer could help reduce the toxic side effects of radionuclide therapy. In vitro experiments were conducted to determine whether NaI 131 can inhibit platinum resistance in A549/DDP cells, which are cisplatin-resistant non-small cell lung cancer cells, and whether gambogic acid (GA) is an effective NaI 131 radiosensitizer. Cell proliferation following drug intervention was analyzed using MTT and isobolographic analysis. Apoptosis was assessed by flow cytometry. In addition, the mechanisms of drug intervention were analyzed by measuring the expression of P-glycoprotein (P-gP), B cell lymphoma 2 (Bcl-2), Bcl2-associated X protein (Bax) and P53 using western blot analysis and immunocytochemistry. According to isobolographic analysis, a low concentration of NaI 131 combined with GA had a synergistic effect on the inhibition of A549/DDP cell proliferation, which was consistent with an increased rate of apoptosis. Furthermore, the overexpression of Bax, and the downregulation of P-gP, P53 and Bcl-2 observed demonstrated the potential mechanism(s) of NaI 131 and GA intervention. NaI 131 may induce apoptosis in A549/DDP cells by regulating apoptosis-related proteins. A low concentration combination of NaI 131 and GA was able to significantly inhibit A549/DDP cell proliferation and induce cell apoptosis. Thus, the two drugs appear to have a synergistic effect on apoptosis of A549/DDP cells.

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confidence: 86%

Role of gambogic acid and NaI131 in A549/DDP cells

et al. 2016

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“…Caspase-3 is activated in the apoptotic cell both by extrinsic and intrinsic pathways directly or indirectly by Caspase-8, 9, 10, and 12, finally to initiate apoptosis (Xiao e t al., 2013;Yamaguchi, 2013). No alteration in Caspase-8 and Caspase-12 expression also supported this datum.…”

Section: Discussionmentioning

confidence: 55%

Effects of Parafibromin Expression on the Phenotypes and Relevant Mechanisms in the DLD-1 Colon Carcinoma Cell Line

Zhao¹,

Sun²,

Zhu³

et al. 2013

Asian Pacific Journal of Cancer Prevention

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Background: Parafibromin is a protein encoded by the HRPT2 (hyperparathyroidism 2) oncosuppressor gene and its down-regulated expression is involved in pathogenesis of parathyroid, breast, gastric and colorectal carcinomas. This study aimed to clarify the effects of parafibromin expression on the phenotypes and relevant mechanisms of DLD-1 colon carcinoma cells. Methods: DLD-1 cells transfected with a parafibromin-expressing plasmid were subjected to examination of phenotype, including proliferation, differentiation, apoptosis, migration and invasion. Phenotype-related proteins were measured by Western blot. Parafibromin and ki-67 expression was detected by immunohistochemistry on tissue microarrays. Results: The transfectants showed higher proliferation by CCK-8, better differentiation by electron microscopy and ALP activity and more apoptotic resistance to cisplatin by DNA fragmentation than controls. There was no difference in early apoptosis by annexin V, capase-3 activity, migration and invasion between DLD-1 cells and their transfectants. Ectopic parafibromin expression resulted in down-regulated expression of smad4, MEKK, GRP94, GRP78, GSK3β-ser9, and Caspase-9. However, no difference was detectable in caspase-12 and -8 expression. A positive relationship was noted between parafibromin and ki-67 expression in colorectal carcinoma. Conclusions: Parafibromin overexpression could promote cell proliferation, apoptotic resistance, and differentiation of DLD-1 cells.

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“…In addition, Bcl-2 is a recognized repressor of the release of cytochrome c to the cytosol [36], inhibiting the formation of the apoptosome and, consequently, the activation of caspase-9. In fact, it has been pointed out that RGN turn the cells more resistant to apoptosis [63]. Recently, we demonstrated that the overexpression of RGN protects testicular cells from apoptosis induced by thapsigargin or actinomycin D, supporting its role as a germ cell survival factor alone or as a mediator in androgen signaling pathways [12].…”

Section: Accepted Manuscriptmentioning

confidence: 62%