Regulation of macroautophagy in ovarian cancer cells in vitro and in vivo by controlling Glucose regulatory protein 78 and AMPK

Kandala, Prabodh K.; Srivastava, Sanjay

doi:10.18632/oncotarget.483

Cited by 59 publications

(55 citation statements)

References 36 publications

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“…The level of tumoricidal activity of binase in the melanoma model is comparable with the effects of some experimental chemotherapeutics, for example, inhibitor of the MAPK-interacting kinases, 33 pro-apoptotic inductor diindolylmethanechimeric, 34 antibodies against PRL-3 35 and the resorcinylicisoxazole/pyrazole HSP90 inhibitors, 36 which demonstrate the ability to suppress tumor and metastasis growth in the nude mice with xerograph melanoma. Our results unambiguously show that binase therapy on animals bearing tumors of different histological types leads to effective retardation of primary tumor and metastasis growth and along with it has general systemic, immunomodulatory and "hepatoprotective" effects.…”

Section: Discussionmentioning

confidence: 52%

Ribonuclease binase inhibits primary tumor growth and metastases via apoptosis induction in tumor cells

et al. 2013

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Section: Discussionmentioning

confidence: 52%

Ribonuclease binase inhibits primary tumor growth and metastases via apoptosis induction in tumor cells

et al. 2013

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“…Moreover, DIM efficiently increased ER stress regulators such as glucose-related protein78 (Grp78), IRE1 and GADD153. A cytosolic calcium chelator BAPT-AM inhibited the phosphorylation of AMPK and also diminished DIM-induced autophagy (Kandala and Srivastava 2012). Inhibitors of AMPK hindered the stimulation of LC3B (light chain-3B) or p62 (nucleoporin 62), indicating that AMPK was necessary in autophagy triggered by DIM.…”

Section: Ampk As a Target To Control Cancer Growth And Treatment Sensmentioning

confidence: 98%

“…Treatment of SKOV-3, OVCAR-3 and TOV-21G ovarian tumor cells with diindolylmethane (DIM) for 24 h induced a concentration-dependent autophagy and DIM augmented levels of LC3B, p62 and Atg12 proteins, which increase during autophagic apoptosis (Kandala and Srivastava 2012). Autophagy-blocking agent bafilomycin or chloroquine abolished autophagy triggered by DIM.…”

Section: Ampk As a Target To Control Cancer Growth And Treatment Sensmentioning

confidence: 99%

A Metabolic Inhibitory Cocktail for Grave Cancers: Metformin, Pioglitazone and Lithium Combination in Treatment of Pancreatic Cancer and Glioblastoma Multiforme

Elmacı

Altinöz²

2016

Biochem Genet

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Pancreatic cancer (PC) and glioblastoma multiforme (GBM) are among the human cancers with worst prognosis which require an urgent need for efficient therapies. Here, we propose to apply to treat both malignancies with a triple combination of drugs, which are already in use for different indications. Recent studies demonstrated a considerable link between risk of PC and diabetes. In experimental models, anti-diabetogenic agents suppress growth of PC, including metformin (M), pioglitazone (P) and lithium (L). L is used in psychiatric practice, yet also bears anti-diabetic potential and selectively inhibits glycogen synthase kinase-3 beta (GSK-3β). M, a biguanide class anti-diabetic agent shows anticancer activity via activating AMP-activated protein kinase (AMPK). Glitazones bind to PPAR-γ and inhibit NF-κB, triggering cell proliferation, apoptosis resistance and synthesis of inflammatory cytokines in cancer cells. Inhibition of inflammatory cytokines could simultaneously decrease tumor growth and alleviate cancer cachexia, having a major role in PC mortality. Furthermore, mutual synergistic interactions exist between PPAR-γ and GSK-3β, between AMPK and GSK-3β and between AMPK and PPAR-γ. In GBM, M blocks angiogenesis and migration in experimental models. Very noteworthy, among GBM patients with type 2 diabetes, usage of M significantly correlates with better survival while reverse is true for sulfonylureas. In experimental models, P synergies with ligands of RAR, RXR and statins in reducing growth of GBM. Further, usage of P was found to be lesser in anaplastic astrocytoma and GBM patients, indicating a protective effect of P against high-grade gliomas. L is accumulated in GBM cells faster and higher than in neuroblastoma cells, and its levels further increase with chronic exposure. Recent studies revealed anti-invasive potential of L in GBM cell lines. Here, we propose that a triple-agent regime including drugs already in clinical usage may provide a metabolic adjuvant therapy for PC and GBM.

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“…Following DNA damage, GADD153 expression is increased, and cells are unable to progress through the cell cycle and exhibit decreased viability. If damage continues, GADD153 may induce apoptosis (23). GADD153 has increased expression and is accompanied by inhibiting the viability of the human ovarian cancer cell line CAOV3.…”

Section: Discussionmentioning

confidence: 99%

“…GADD153 has increased expression and is accompanied by inhibiting the viability of the human ovarian cancer cell line CAOV3. Cell cycle arrest, triggered by GADD153, prevents cells progressing from G 1 to S phase and occurs in numerous apoptotic cells (23). This indicates that long-term starvation results in damage to DNA, inducing increased expression of GADD153 and results in decreased cell viability (24).…”

Section: Discussionmentioning

confidence: 99%

Hesperidin inhibits ovarian cancer cell viability through endoplasmic reticulum stress signaling pathways

Zhao

Gao

et al. 2017

Oncol Lett

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Abstract. Hesperidin is a vitamin P flavonoid compound primarily present in citrus fruits. The aim of the present study was to investigate whether hesperidin inhibits ovarian cancer cell viability via endoplasmic reticulum stress signaling pathways. A2780 cells were treated with various doses of hesperidin for 6, 12 or 24 h, and the viability of A2780 cells was assessed using the MTT assay. Hesperidin decreased the viability of A2780 cells and increased cytotoxicity in a doseand time-dependent manner. In addition, hesperidin induced apoptosis and increased cleaved caspase-3 protein expression levels in A2780 cells. Furthermore, hesperidin markedly increased the protein expression of anti-growth arrest-and DNA damage-inducible gene 153, anti-CCAAT'enhancer-binding protein homologous protein, glucose-regulated protein 78 and cytochrome c in A2780 cells. The results of the present study indicated that hesperidin inhibits cell viability and induces apoptosis in ovarian cancer cells via endoplasmic reticulum stress signaling pathways. Thus, hesperidin may offer a novel therapeutic tool for ovarian carcinoma.

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Regulation of macroautophagy in ovarian cancer cells in vitro and in vivo by controlling Glucose regulatory protein 78 and AMPK

Abstract: ABSTRACT:In this study we show that diindolylmethane (

Cited by 59 publications

References 36 publications

Ribonuclease binase inhibits primary tumor growth and metastases via apoptosis induction in tumor cells

Ribonuclease binase inhibits primary tumor growth and metastases via apoptosis induction in tumor cells

A Metabolic Inhibitory Cocktail for Grave Cancers: Metformin, Pioglitazone and Lithium Combination in Treatment of Pancreatic Cancer and Glioblastoma Multiforme

Hesperidin inhibits ovarian cancer cell viability through endoplasmic reticulum stress signaling pathways

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