R(h)oad to antitumour therapy.

R(h)oad to antitumour therapy.
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DOI:
10.1002/ctd2.160
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发表时间:
2022-12
期刊:
Clinical and translational discovery
影响因子:
--
通讯作者:
Viviane Nascimento Da Conceicao;B. B. Mishra-B.;Brij B. Singh
Viviane Nascimento Da Conceicao;B. B. Mishra-B.;Brij B. Singh
中科院分区:
其他
文献类型:
--
作者:
Viviane Nascimento Da Conceicao;B. B. Mishra-B.;Brij B. Singh

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Autophagy, an evolutionarily intracellular degradation catabolic process maintains cellular homeostasis during stress conditions to recycles nutrients from damaged organelles1, 2. Importantly, although autophagy plays a dual role in tumor promotion and suppression in many cancers, inhibition of autophagy plays a vital role in cancer immunotherapy. Studies have showed that altering the autophagic process by inhibiting or inducing can promote the effectiveness of immunotherapy3, 4. Immunogenic cell death (ICD) is a distinctive immune response induced by anticancer chemotherapeutics resulting in cell death inducted by cellular stress and eventually release of DAMPs (damage-associated molecular patterns) 5, 6. Pharmacology inducing ICD activates autophagy in tumor cells, that together with radiotherapy/chemotherapy boosts efficacy by promoting ICD7.In their letter to editor, Yang and collaborators (Yang et al., In press) propose that pharmacological enhancement in the autophagy process can be effective in boosting anticancer immune responses to immunogenic cell death drugs8, 9. They propose that ginsenoside Rh2 (G-Rh2) heightened the MTX (mitoxantrone)-induced ICD including ATP release increase, discharge of HMGB1 (high mobility group box 1) and repositioning of calreticulin (CALR) to the membrane enhancing anti-tumor immune responses (Figure 1). G-Rh2 are ginsenosides, the main components from ginseng and proved to have pharmacological anti-cancer capabilities, inducing autophagy by activating transcriptional factors EB (TFEB) and E3 (TFE3) which adds to the collaborative effect of G-Rh2 that together with the chemotherapy drug MTX activates ATP release10, 11.