Glucose starvation-induced oxidative stress causes mitochondrial dysfunction and apoptosis via Prohibitin 1 upregulation in human breast cancer cells

Raut, Ganesh Kumar; Chakrabarti, Moumita; Pamarthy, Deepika; Bhadra, Manika Pal

doi:10.1016/j.freeradbiomed.2019.09.020

Cited by 49 publications

(31 citation statements)

References 69 publications

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“…As diet can also play a role in the UPR maintenance 53,80 , we subjected worms to different forms of starvation. When C. elegans are starved during the L1 larval stage, they enter L1 arrest, which halts the development and reproductive growth, enhances stress resistance, modifies feeding behavior, and alters metabolic flux 81,82 .…”

Section: Discussionmentioning

confidence: 99%

“…Starvation during the L4 larval and adult stages has beneficial effects such as extended life span, germline cell reduction, delayed reproduction, and thermotolerance 83 . At the cellular level, starvation induces both mitochondrial and ER stress 53,80,84 . Mitochondria become fragmented in starved animals and are cleared through mitophagy 10,80,85 .…”

Section: Discussionmentioning

confidence: 99%

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C. elegans electrotaxis behavior is modulated by heat shock response and unfolded protein response signaling pathways

Taylor

Minhas

Tong

et al. 2021

Sci Rep

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The nematode C. elegans is a leading model to investigate the mechanisms of stress-induced behavioral changes coupled with biochemical mechanisms. Our group has previously characterized C. elegans behavior using a microfluidic-based electrotaxis device, and showed that worms display directional motion in the presence of a mild electric field. In this study, we describe the effects of various forms of genetic and environmental stress on the electrotactic movement of animals. Using exposure to chemicals, such as paraquat and tunicamycin, as well as mitochondrial and endoplasmic reticulum (ER) unfolded protein response (UPR) mutants, we demonstrate that chronic stress causes abnormal movement. Additionally, we report that pqe-1 (human RNA exonuclease 1 homolog) is necessary for the maintenance of multiple stress response signaling and electrotaxis behavior of animals. Further, exposure of C. elegans to several environmental stress-inducing conditions revealed that while chronic heat and dietary restriction caused electrotaxis speed deficits due to prolonged stress, daily exercise had a beneficial effect on the animals, likely due to improved muscle health and transient activation of UPR. Overall, these data demonstrate that the electrotaxis behavior of worms is susceptible to cytosolic, mitochondrial, and ER stress, and that multiple stress response pathways contribute to its preservation in the face of stressful stimuli.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

C. elegans electrotaxis behavior is modulated by heat shock response and unfolded protein response signaling pathways

Taylor

Minhas

Tong

et al. 2021

Sci Rep

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“…Glucose starvation of MDA-MB-231 and MCF-7 breast cancer cells provoked a decreased mitochondrial respiration. Glucose starvation also sensitized MDA-MB-231 cells to apoptosis and decreased their migratory potential [51].…”

Section: Targeting Glycolysis and Oxphosmentioning

confidence: 99%

“…Tumour cells can alter their redox balance and deregulate redox signalling to support malignant progression and to gain resistance to treatment [51]. They increase their antioxidant capacity to counterbalance the increased production of ROS [52,53], which permits them to generate high levels of ROS to activate proximal signalling pathways that promote proliferation and would not otherwise induce cancer cell death or senescence.…”

Section: Targeting Mitochondrial Redox Signalling Pathways and Ros Homentioning

confidence: 99%

Mitocans Revisited: Mitochondrial Targeting as Efficient Anti-Cancer Therapy

Dong

Gopalan

Holland

et al. 2020

IJMS

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Mitochondria are essential cellular organelles, controlling multiple signalling pathways critical for cell survival and cell death. Increasing evidence suggests that mitochondrial metabolism and functions are indispensable in tumorigenesis and cancer progression, rendering mitochondria and mitochondrial functions as plausible targets for anti-cancer therapeutics. In this review, we summarised the major strategies of selective targeting of mitochondria and their functions to combat cancer, including targeting mitochondrial metabolism, the electron transport chain and tricarboxylic acid cycle, mitochondrial redox signalling pathways, and ROS homeostasis. We highlight that delivering anti-cancer drugs into mitochondria exhibits enormous potential for future cancer therapeutic strategies, with a great advantage of potentially overcoming drug resistance. Mitocans, exemplified by mitochondrially targeted vitamin E succinate and tamoxifen (MitoTam), selectively target cancer cell mitochondria and efficiently kill multiple types of cancer cells by disrupting mitochondrial function, with MitoTam currently undergoing a clinical trial.

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“…Cancer is a proliferative disease of multicellular organisms. Similar to parasites, cancer cells manipulate the metabolism of the host organism, thereby receiving a larger portion of glucose than the host cells (1,2). To prevent glucose starvation dangerous to such glucose-sensitive organs as the brain, the host organism uses glucose sensors capable of maintaining normoglycemia in response to deficient or excess glucose (3).…”

Section: Introductionmentioning

confidence: 99%

A View on Pathogenesis of ≪Vicious Cancer Progression Cycle≫

Schwartsburd

2020

Front. Oncol.

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Unrestricted tumor growth requires a permanent supply of glucose that can be obtained from cancer-stimulated hepatic glucose production and/or glucose redirecting from host insulin resistant tissues to cancer cells. This study proposes a mechanism based on metabolic and hormonal changes that may provoke glucose delivery to cancer cells through two interconnected "vicious cycles" whose continuous activity drives cancer progression. As follows from the proposed here feedback model, these "vicious cycles" result from cancer-mediated manipulation of host glucose sensors. The derived conclusions contribute to a better understanding of cancer pathogenesis and identifying potential therapeutic targets.

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Glucose starvation-induced oxidative stress causes mitochondrial dysfunction and apoptosis via Prohibitin 1 upregulation in human breast cancer cells

Cited by 49 publications

References 69 publications

C. elegans electrotaxis behavior is modulated by heat shock response and unfolded protein response signaling pathways

C. elegans electrotaxis behavior is modulated by heat shock response and unfolded protein response signaling pathways

Mitocans Revisited: Mitochondrial Targeting as Efficient Anti-Cancer Therapy

A View on Pathogenesis of ≪Vicious Cancer Progression Cycle≫

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