Heme Oxygenase-1 Promotes Survival of Renal Cancer Cells through Modulation of Apoptosis- and Autophagy-regulating Molecules

Banerjee, Prashant; Basu, Aninda; Węgiel, Barbara; Otterbein, Leo E.; Mizumura, Kenji; Gasser, Martin; Waaga-Gasser, Ana Maria; Choi, Augustine M.K.; Pal, Soumitro

doi:10.1074/jbc.m112.393140

Cited by 75 publications

(84 citation statements)

References 49 publications

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“…Currently, the role of autophagy in kidney disease remains controversial, as it is involved in both cell survival and death depending on different stimuli or cellular environment. 12,52 Our study provides in vitro and in vivo evidence that sustained HG resulted in defective autophagy in glomerulus and podocyte, which could be partially corrected by UDCA or 4-PBA treatment.…”

Section: Discussionmentioning

confidence: 94%

Ursodeoxycholic acid and 4-phenylbutyrate prevent endoplasmic reticulum stress-induced podocyte apoptosis in diabetic nephropathy

Wang

Chen

et al. 2016

Laboratory Investigation

100

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Endoplasmic reticulum (ER) stress, resulting from the accumulation of misfolded and/or unfolded proteins in ER membranes, is involved in the pathogenesis of diabetic nephropathy (DN). The aim of this study was to investigate the role of ER stress inhibitors ursodeoxycholic acid (UDCA) and 4-phenylbutyrate (4-PBA) in the treatment of DN in db/db mice. Findings have revealed that diabetic db/db mice were more hyperglycemic than their non-diabetic controls, and exhibited a marked increase in body weight, water intake, urine volume, fasting plasma glucose, systolic blood pressure, glucose and insulin tolerance. UDCA (40 mg/kg/day) or 4-PBA (100 mg/kg/day) treatment for 12 weeks resulted in an improvement in these biochemical and physical parameters. Moreover, UDCA or 4-PBA intervention markedly decreased urinary albuminuria and attenuated mesangial expansion in diabetic db/db mice, compared with db/db mice treated with vehicle. These beneficial effects of UDCA or 4-PBA on DN were associated with the inhibition of ER stress, as evidenced by the decreased expression of BiP, phospho-IRE1α, phospho-eIF2α, CHOP, ATF-6 and spliced X-box binding protein-1 in vitro and in vivo. UDCA or 4-PBA prevented hyperglycemia-induced or high glucose (HG)-induced apoptosis in podocytes in vivo and in vitro via the inhibition of caspase-3 and caspase-12 activation. Autophagy deficiency was also seen in glomeruli in diabetic mice and HG-incubated podocytes, exhibiting decreased expression of LC3B and Beclin-1, which could be restored by UDCA or 4-PBA treatment. Taken together, our results have revealed an important role of ER stress in the development of DN, and UDCA or 4-PBA treatment may be a potential novel therapeutic approach for the treatment of DN.

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Section: Discussionmentioning

confidence: 94%

Ursodeoxycholic acid and 4-phenylbutyrate prevent endoplasmic reticulum stress-induced podocyte apoptosis in diabetic nephropathy

Wang

Chen

et al. 2016

Laboratory Investigation

100

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“…The therapeutic efficacy of these drugs may be linked, at least in part, to HO-1 induction (reviewed in Dunn et al 2014). HO-1 expression in human renal cancer cells was induced by anti-renal cancer drugs rapamycin and sorafenib (Banerjee et al 2012). Intriguingly, a wide range of dietary antioxidants of plant origin such as curcumin, quercetin, tert-butylhydroquinone and caffeic acid phenethyl ester are HO-1 inducers so are catechin (in green tea), α-lipoic acid (in broccoli, spinach), resveratrol (in red wine, grapes), carnosol, sulphoraphane (cruciferous vegetable), coffee diterpenes cafestol and kahwoel (reviewed in Durante 2010).…”

Section: Ho-1 Induction By Therapeutic Drugs and Plant Antioxidantsmentioning

confidence: 99%

“…This demonstrates an indispensable role for HO-1 in the survival of the PT cells. Increased HO-1 expression in renal cancer cells promoted their survival and resistance to apoptosis (Banerjee et al 2012).…”

Section: Modulation Of Cadmium Toxicity By a Stress Response Mechanismmentioning

confidence: 99%

Kidney Cadmium Toxicity, Diabetes and High Blood Pressure: The Perfect Storm

Satarug

Vesey

Gobé

2017

Tohoku J. Exp. Med.

102

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“…(Vinken et al, 2013;Banerjee et al, 2012;Zhu et al, 2014). Previous studies have shown that Lamellarin D is an alkaloid capable of inhibiting a variety of human tumors and has important significance in the treatment of tumors (Banerjee et al, 2012). By observing the effects of Lamellarin D on human leukemia K562 cells, this study found that Lamellarin D significantly inhibited tumor cell proliferation, induced apoptosis, and arrested cell cycle in G0/G1 phase.…”

Section: Discussionmentioning

confidence: 72%

“…Elucidation of the mechanisms of drug-mediated inhibition on tumor cell growth and proliferation has important significance for the treatment of tumors and the improvement of prognosis and there was a decreased mRNA and protein expression of tumor related gene such as CDK1, Survivin, Bcl-2 and so on. (Vinken et al, 2013;Banerjee et al, 2012;Zhu et al, 2014). Previous studies have shown that Lamellarin D is an alkaloid capable of inhibiting a variety of human tumors and has important significance in the treatment of tumors (Banerjee et al, 2012).…”

Section: Discussionmentioning

confidence: 99%

Inhibition Effects of Lamellarin D on Human Leukemia K562 Cell Proliferation and Underlying Mechanisms

Zhang¹,

Wang²,

Zhu³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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Lamellarin D (LamD) is a marine alkaloid with a pronounced cytotoxicity against a large panel of cancer cells, affecting cell growth and inducing apoptosis. However, the molecular mechanisms of action of this compound are poorly understood. In this study, the anticancer efficacy of LamD was investigated in human leukemia K562 cells. The results showed suppressed cell proliferation and induction of G0/G1-phase arrest,while expression of CDK1, and activity of smad3 and smad5 were reduced, but that of p27, p53 and STGC3 was increased. LamD induced cell apoptosis through activation of caspases-8/-3, inhibition of survivin and Bcl-2, suggesting that this compound may also act through a caspase-independent pathway. Moreover, LamD inhibited the secretion of TGF-β, IL-1β, IL-6, IL-8 and other inflammatory cytokines and the transcriptional activity of transcription factor NF-κB in human leukemia K562 cells.Taken together, our results suggest that LamD-mediated inhibition of leukemia cell proliferation may be related to the induction of apoptosis and the regulation of cell cycle, tumorrelated gene expression and cytokine expression, which may provide a new way of thinking for the treatment leukemia.

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Heme Oxygenase-1 Promotes Survival of Renal Cancer Cells through Modulation of Apoptosis- and Autophagy-regulating Molecules

Cited by 75 publications

References 49 publications

Ursodeoxycholic acid and 4-phenylbutyrate prevent endoplasmic reticulum stress-induced podocyte apoptosis in diabetic nephropathy

Ursodeoxycholic acid and 4-phenylbutyrate prevent endoplasmic reticulum stress-induced podocyte apoptosis in diabetic nephropathy

Kidney Cadmium Toxicity, Diabetes and High Blood Pressure: The Perfect Storm

Inhibition Effects of Lamellarin D on Human Leukemia K562 Cell Proliferation and Underlying Mechanisms

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