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Hydroxychloroquine activates apoptotic process. 87 / 87
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"Application of the autophagy inhibitor, hydroxychloroquine (HCQ) (10 microM), promoted apoptosis of primary HCC cells under hypoxic cultivation and 5-FU treatment, as evidenced by the increased expression of cleaved caspase-3 and cleaved caspase-8 (XREF_FIG) and inhibition of proliferation, as measured via MTT assays (XREF_FIG)."
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"These effects were blocked by bafilomycin A1, which prevents degradation of LC3, induces its accumulation in autophagolysosomes [66] and acts as an inhibitor of the vacuolar-type H+-ATPase, changing endosomal pH [67], showing that hydroxychloroquine activated apoptosis via lysosomes instead of other organelles (mitochondria or nuclei, for example)."
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"Additionally, HCQ induces apoptosis of autoreactive T-cells and interferes with antigen processing by B-cells, thereby interfering with their functions and cytokine production (interleukin [IL]-1, IL-6, interferon-gamma, tumour necrosis factor [TNF], and B-cell activating factor) [XREF_BIBR, XREF_BIBR]."
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"Since there is evidence that HCQ has a potential application in cancer treatment for its inhibition of autophagy in leukemic, breast cancer MCF-7 and melanoma cells and may subsequently induce their apoptosis, this process may also be important to the actions of HCQ in cervical cancer cells."
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"The hypothesis that CQ might afford Ebola prophylaxis comes from our own work showing hydroxychloroquine (HCQ) induces apoptosis (programmed cell death) in peripheral blood mononuclear cells.2 HCQ also inhibits the replication of HIV in vitro.3There is a possible clinical analogy."
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"In addition, HCQ activated ATM to enhance HR repair, a high-fidelity repair for DNA double-strand breaks (DSBs) in cells, while BKM120 inhibited HR repair by blocking the phosphorylation of ATM and the expression of BRCA1/2 and Rad51.Our study revealed that HCQ and BKM120 synergistically increased DSBs in tumor cells and therefore augmented apoptosis, resulting in enhanced antitumor efficacy."
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"ese effects were blocked by bafilomycin A1, which prevents degradation of LC3, induces its accumulation in autophagolysosomes [66] and acts as an inhibitor of the vacuolar-type H + -ATPase, changing endosomal pH [67] , showing that hydroxychloroquine activated apoptosis via lysosomes instead of other organelles (mitochondria or nuclei, for example)."
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"HCQ alone produced decreased cell growth and induction of caspase-dependent apoptosis in all S45F mutated DT cells tested but had no effect in T41A-mutated DT cells, confirming our previous results that S45F-mutated DT cell strains are highly dependent on autophagy instead of apoptosis."