<i>ATG5</i> knockout promotes paclitaxel sensitivity in drug-resistant cells <i>via</i> induction of necrotic cell death

Hwang, Sung‐Hee; Yeom, Hojin; Lee, Michael

doi:10.4196/kjpp.2020.24.3.233

Cited by 6 publications

(3 citation statements)

References 46 publications

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“…Recently, ATG5 has been found to be implicated in doxorubicin resistance in gall bladder cancer [523]. It has been shown that knocking down ATG5 in paclitaxel-resistant cells causes a G2/M arrest and makes cells susceptible to paclitaxel-induced necrosis [524]. Another study showed that direct knockdown of ATG5 increased paclitaxel resistance in Ras-NIH 3T3 (v-Ha-ras-transformed NIH 3T3) cells by reducing the frequency of early apoptotic cells [525].…”

Section: Autophagy Acts As a Chemotherapy Resistance Machinery In The...mentioning

confidence: 99%

Chemotherapy Resistance: Role of Mitochondrial and Autophagic Components

Bahar

Han

Kim

et al. 2022

Cancers

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Cancer chemotherapy resistance is one of the most critical obstacles in cancer therapy. One of the well-known mechanisms of chemotherapy resistance is the change in the mitochondrial death pathways which occur when cells are under stressful situations, such as chemotherapy. Mitophagy, or mitochondrial selective autophagy, is critical for cell quality control because it can efficiently break down, remove, and recycle defective or damaged mitochondria. As cancer cells use mitophagy to rapidly sweep away damaged mitochondria in order to mediate their own drug resistance, it influences the efficacy of tumor chemotherapy as well as the degree of drug resistance. Yet despite the importance of mitochondria and mitophagy in chemotherapy resistance, little is known about the precise mechanisms involved. As a consequence, identifying potential therapeutic targets by analyzing the signal pathways that govern mitophagy has become a vital research goal. In this paper, we review recent advances in mitochondrial research, mitophagy control mechanisms, and their implications for our understanding of chemotherapy resistance.

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Section: Autophagy Acts As a Chemotherapy Resistance Machinery In The...mentioning

confidence: 99%

Chemotherapy Resistance: Role of Mitochondrial and Autophagic Components

Bahar

Han

Kim

et al. 2022

Cancers

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“…These data suggest that the difference in PTX sensitivity between ATG5 KO and their parental cells may result from the disparity in the proportions of necrotic cells in both populations. Thus, these results demonstrate that the ATG5 KO in multidrug-resistant cells leads to a marked G2/M arrest and sensitizes cells to PTX-induced necrosis [106].…”

Section: Nonapoptotic Forms Of Cell Death Induced By Taxanesmentioning

confidence: 51%

Platinum drugs and taxanes: can we overcome resistance?

et al. 2021

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Cancer therapy is aimed at the elimination of tumor cells and acts via the cessation of cell proliferation and induction of cell death. Many research publications discussing the mechanisms of anticancer drugs use the terms “cell death” and “apoptosis” interchangeably, given that apoptotic pathways are the most common components of the action of targeted and cytotoxic compounds. However, there is sound evidence suggesting that other mechanisms of drug-induced cell death, such as necroptosis, ferroptosis, autophagy, etc. may significantly contribute to the fate of cancer cells. Molecular cross-talks between apoptotic and nonapoptotic death pathways underlie the successes and the failures of therapeutic interventions. Here we discuss the nuances of the antitumor action of two groups of the widely used anticancer drugs, i.e., platinum salts and taxane derivatives. The available data suggest that intelligent interference with the choice of cell death pathways may open novel opportunities for cancer treatment.

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“…Then, the vector was transfected into PC12 cells using Lipofectamine 3000 transfection reagent (L3000075, Thermo), and stable expression cells were screened using 800 μg/ml G418 (G8160, Solarbio). The NLRC3 knockdown vector was constructed according to a previous study [13]. Pairs of oligos were obtained using the following primers: Forward: 5'-CACCGTCAGACTTCTGTTGACCAAG-3', Reverse: 5'-AACCTTGGTCAACAGAAGTCTGAC-3', and oligos were incubated with T4 PNK (M0201S, NEB) at 37°C for 30 min and 95°C for 5 min.…”

Section: Vector Constructionmentioning

confidence: 99%

Overexpression of NLRC3 enhanced inhibition effect of sevoflurane on inflammation in an ischaemia reperfusion cell model

Li¹,

Hu²,

Xu³

2020

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Brain ischaemia is one of the leading causes of mortality and disability worldwide, and the damage caused by ischaemia not only induces primary damage but also that induced by ischaemia-reperfusion (I/R) injury. Multiple processes including inflammation and oxidative stress response play important roles in the development of brain ischaemia injury. Sevoflurane is a well-known volatile anaesthetic, and a recent study discovered the role of sevoflurane in suppression of the inflammation response process via inhibition of inflammatory infiltrates and production, maintaining the balance of cytokine responses, although the possible mechanism was not fully clear. NLRC3 is a member of the nucleotide-binding domain and leucine-rich repeat containing (NLR) family, and it has been regarded as a regulator of the inflammation process via the regulation of inflammasome formation, which is an initiator of inflammatory events. In the present study, we found that overexpression of NLRC3 reduced the apoptosis in a cellular model of ischaemia reperfusion, and the expression of pro-inflammatory cytokines was also decreased. Further study found that these effects might be mediated by the TRAF6/TLR4/NF-κB signalling pathway. Thus, we speculate that overexpression might enhance the effect of sevoflurane in inhibiting the inflammatory response process in an ischaemia reperfusion model, which might be a new therapeutic strategy.

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ATG5 knockout promotes paclitaxel sensitivity in drug-resistant cells via induction of necrotic cell death

Cited by 6 publications

References 46 publications

Chemotherapy Resistance: Role of Mitochondrial and Autophagic Components

Chemotherapy Resistance: Role of Mitochondrial and Autophagic Components

Platinum drugs and taxanes: can we overcome resistance?

Overexpression of NLRC3 enhanced inhibition effect of sevoflurane on inflammation in an ischaemia reperfusion cell model

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