AGE/RAGE axis regulates reversible transition to quiescent states of ALK-rearranged NSCLC and pancreatic cancer cells in monolayer cultures

Kadonosono, Tetsuya; Miyamoto, K.; Sakai, Shiori; Matsuo, Yoshiyuki; Kitajima, Shojiro; Wang, Qiannan; Endo, Makoto; Niibori, Mizuho; Kuchimaru, Takahiro; Soga, Tomoyoshi; Hirota, Kaoru; Kizaka‐Kondoh, Shinae

doi:10.1038/s41598-022-14272-0

Cited by 7 publications

(3 citation statements)

References 40 publications

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“…An increase in cellular ROS is the most common promoter of these three processes. Genomic instability is mediated by an increase in ROS levels and damage to nuclear nucleosides and inducing minority MOMP (mitochondrial outer membrane permeabilization) [ 10 ]; quiescence evasion is conducted by an increase in cellular ROS and following the activation of the Ras pathway [ 29 , 30 ]; Section 3 summarizes how mitochondria are involved in EMT. ROS is a double-edged sword, destroying cancer cells at high levels and promoting cancer progression at moderate levels.…”

Section: The Pivotal Role Of Mitochondria In Cancer Cells’ Metabolismmentioning

confidence: 99%

Mitochondrial Metabolism: A New Dimension of Personalized Oncology

Behnam

Taghizadeh‐Hesary

2023

Cancers

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Energy is needed by cancer cells to stay alive and communicate with their surroundings. The primary organelles for cellular metabolism and energy synthesis are mitochondria. Researchers recently proved that cancer cells can steal immune cells’ mitochondria using nanoscale tubes. This finding demonstrates the dependence of cancer cells on normal cells for their living and function. It also denotes the importance of mitochondria in cancer cells’ biology. Emerging evidence has demonstrated how mitochondria are essential for cancer cells to survive in the harsh tumor microenvironments, evade the immune system, obtain more aggressive features, and resist treatments. For instance, functional mitochondria can improve cancer resistance against radiotherapy by scavenging the released reactive oxygen species. Therefore, targeting mitochondria can potentially enhance oncological outcomes, according to this notion. The tumors’ responses to anticancer treatments vary, ranging from a complete response to even cancer progression during treatment. Therefore, personalized cancer treatment is of crucial importance. So far, personalized cancer treatment has been based on genomic analysis. Evidence shows that tumors with high mitochondrial content are more resistant to treatment. This paper illustrates how mitochondrial metabolism can participate in cancer resistance to chemotherapy, immunotherapy, and radiotherapy. Pretreatment evaluation of mitochondrial metabolism can provide additional information to genomic analysis and can help to improve personalized oncological treatments. This article outlines the importance of mitochondrial metabolism in cancer biology and personalized treatments.

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Section: The Pivotal Role Of Mitochondria In Cancer Cells’ Metabolismmentioning

confidence: 99%

Mitochondrial Metabolism: A New Dimension of Personalized Oncology

Behnam

Taghizadeh‐Hesary

2023

Cancers

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“…Reversible, plastic resistance in prostate, breast, colon, pancreatic, and non-small cell lung cancer cell line models has been shown to be a consequence of nutrient deprivation which introduces ROS and low cell proliferation, priming cells to adapt to anti-tumor agents such as the mitochondrial ETC Complex I inhibitor metformin ( Marini et al, 2016 ; White et al, 2020 ; Kadonosono et al, 2022 ). To capitalize on this adaptation, cancers such as colon or breast could be treated with metabolic inhibitors to prevent oxphos or glycolysis mediated adaptations ( Marini et al, 2016 ).…”

Section: Therapy-induced Rewiring Of Mitochondrial Metabolism: Eviden...mentioning

confidence: 99%

Rewiring of mitochondrial metabolism in therapy-resistant cancers: permanent and plastic adaptations

Pendleton,

Wang,

Echeverria

2023

Front. Cell Dev. Biol.

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Deregulation of tumor cell metabolism is widely recognized as a “hallmark of cancer.” Many of the selective pressures encountered by tumor cells, such as exposure to anticancer therapies, navigation of the metastatic cascade, and communication with the tumor microenvironment, can elicit further rewiring of tumor cell metabolism. Furthermore, phenotypic plasticity has been recently appreciated as an emerging “hallmark of cancer.” Mitochondria are dynamic organelles and central hubs of metabolism whose roles in cancers have been a major focus of numerous studies. Importantly, therapeutic approaches targeting mitochondria are being developed. Interestingly, both plastic (i.e., reversible) and permanent (i.e., stable) metabolic adaptations have been observed following exposure to anticancer therapeutics. Understanding the plastic or permanent nature of these mechanisms is of crucial importance for devising the initiation, duration, and sequential nature of metabolism-targeting therapies. In this review, we compare permanent and plastic mitochondrial mechanisms driving therapy resistance. We also discuss experimental models of therapy-induced metabolic adaptation, therapeutic implications for targeting permanent and plastic metabolic states, and clinical implications of metabolic adaptations. While the plasticity of metabolic adaptations can make effective therapeutic treatment challenging, understanding the mechanisms behind these plastic phenotypes may lead to promising clinical interventions that will ultimately lead to better overall care for cancer patients.

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“…Therefore, one may conclude that quiescence evasion is orchestrated by another transcription factor. Recent evidence on a non-small cell lung cancer (NSCLC) model demonstrated that this process is regulated by Ras, Rap1, PI3K/Akt, and ERK signaling pathway [ 86 ]. Moreover, it has been noted that mitochondria are indexed actors in Ras-mediated cancer proliferation.…”

Section: Mitochondria’s Benefits For Cancer Cellsmentioning

confidence: 99%

Targeted Anti-Mitochondrial Therapy: The Future of Oncology

Taghizadeh‐Hesary

Akbari

Bahadori

et al. 2022

Genes

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Like living organisms, cancer cells require energy to survive and interact with their environment. Mitochondria are the main organelles for energy production and cellular metabolism. Recently, investigators demonstrated that cancer cells can hijack mitochondria from immune cells. This behavior sheds light on a pivotal piece in the cancer puzzle, the dependence on the normal cells. This article illustrates the benefits of new functional mitochondria for cancer cells that urge them to hijack mitochondria. It describes how functional mitochondria help cancer cells’ survival in the harsh tumor microenvironment, immune evasion, progression, and treatment resistance. Recent evidence has put forward the pivotal role of mitochondria in the metabolism of cancer stem cells (CSCs), the tumor components responsible for cancer recurrence and metastasis. This theory highlights the mitochondria in cancer biology and explains how targeting mitochondria may improve oncological outcomes.

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AGE/RAGE axis regulates reversible transition to quiescent states of ALK-rearranged NSCLC and pancreatic cancer cells in monolayer cultures

Cited by 7 publications

References 40 publications

Mitochondrial Metabolism: A New Dimension of Personalized Oncology

Mitochondrial Metabolism: A New Dimension of Personalized Oncology

Rewiring of mitochondrial metabolism in therapy-resistant cancers: permanent and plastic adaptations

Targeted Anti-Mitochondrial Therapy: The Future of Oncology

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