JNK and NFκB dependence of apoptosis induced by vinblastine in human acute promyelocytic leukaemia cells

Calviño, Eva; Tejedor, M. Cristina; Sancho, Pilar; Herráez, Ángel; Diez, José C.

doi:10.1002/cbf.3105

Cited by 8 publications

(4 citation statements)

References 25 publications

(135 reference statements)

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“…Most important signaling pathways are controlled by PI3K, Akt, and the mammalian target of rapamycin (mTOR) (Lefranc and Kiss, 2006). Tumor cell death induced by anticancer drugs is also regulated by various other signaling molecules, including JNK, Erk, c-myc, and NF-kB (Tashiro et al ., 1998; Fan et al ., 2000; Stadheim et al ., 2001; Bressin et al ., 2006; Calvino et al ., 2015). Curcumin activates the P53 signaling pathway by up-regulating P53 and P21, which also inhibit the PI3K pathway by down-regulating PI3K, p-Akt, and p-mTOR (Fu et al ., 2018).…”

Section: Discussionmentioning

confidence: 99%

Curcumin-Induced Autophagy Augments Its Antitumor Effect against A172 Human Glioblastoma Cells

Lee

Yoon

Moon

2019

Biomolecules & Therapeutics

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Glioblastoma is the most aggressive common brain tumor in adults. Curcumin, from Curcuma longa , is an effective antitumor agent. Although the same proteins control both autophagy and cell death, the molecular connections between them are complicated and autophagy may promote or inhibit cell death. We investigated whether curcumin affects autophagy, which regulates curcumin-mediated tumor cell death in A172 human glioblastoma cells. When A172 cells were incubated with 10 μM curcumin, autophagy increased in a time-dependent manner. Curcumin-induced cell death was reduced by co-incubation with the autophagy inhibitors 3-methyladenine (3-MA), hydroxychloroquine (HCQ), and LY294002. Curcumin-induced cell death was also inhibited by co-incubation with rapamycin, an autophagy inducer. When cells were incubated under serum-deprived medium, LC3-II amount was increased but the basal level of cell viability was reduced, leading to the inhibition of curcumin-induced cell death. Cell death was decreased by inhibiting curcumin-induced autophagy using small interference RNA (siRNA) of Atg5 or Beclin1. Therefore, curcumin-mediated tumor cell death is promoted by curcumin-induced autophagy, but not by an increase in the basal level of autophagy in rapamycin-treated or serum-deprived conditions. This suggests that the antitumor effects of curcumin are influenced differently by curcumin-induced autophagy and the prerequisite basal level of autophagy in cancer cells.

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Section: Discussionmentioning

confidence: 99%

Curcumin-Induced Autophagy Augments Its Antitumor Effect against A172 Human Glioblastoma Cells

Lee

Yoon

Moon

2019

Biomolecules & Therapeutics

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“…In a study, the mechanism of anticancer effect of vinblastine on human acute promyelocytic leukemia NB4 cells was reported, and it was found that vinblastine could induce an apoptotic response by downregulating NF-κB expression, sustaining JNK activation, and finally triggering caspase cascade. In addition, it will also cause changes in p53 and DNA fragmentation [ 124 ]. Moreover, hapalindole H (Hap H), extracted from Fischerella muscicola with a median effective concentration (EC 50 ) value of 20 nM, induced toxicity in the PC-3 prostate cancer cells, and it showed potential NF-ĸB p65 inhibitory activity on PC-3 cells, and this inhibition would lead to apoptotic cell death.…”

Section: Targeting Apoptotic Signaling Pathways With Indole Alkaloids...mentioning

confidence: 99%

Naturally derived indole alkaloids targeting regulated cell death (RCD) for cancer therapy: from molecular mechanisms to potential therapeutic targets

et al. 2022

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Regulated cell death (RCD) is a critical and active process that is controlled by specific signal transduction pathways and can be regulated by genetic signals or drug interventions. Meanwhile, RCD is closely related to the occurrence and therapy of multiple human cancers. Generally, RCD subroutines are the key signals of tumorigenesis, which are contributed to our better understanding of cancer pathogenesis and therapeutics. Indole alkaloids derived from natural sources are well defined for their outstanding biological and pharmacological properties, like vincristine, vinblastine, staurosporine, indirubin, and 3,3′-diindolylmethane, which are currently used in the clinic or under clinical assessment. Moreover, such compounds play a significant role in discovering novel anticancer agents. Thus, here we systemically summarized recent advances in indole alkaloids as anticancer agents by targeting different RCD subroutines, including the classical apoptosis and autophagic cell death signaling pathways as well as the crucial signaling pathways of other RCD subroutines, such as ferroptosis, mitotic catastrophe, necroptosis, and anoikis, in cancer. Moreover, we further discussed the cross talk between different RCD subroutines mediated by indole alkaloids and the combined strategies of multiple agents (e.g., 3,10-dibromofascaplysin combined with olaparib) to exhibit therapeutic potential against various cancers by regulating RCD subroutines. In short, the information provided in this review on the regulation of cell death by indole alkaloids against different targets is expected to be beneficial for the design of novel molecules with greater targeting and biological properties, thereby facilitating the development of new strategies for cancer therapy. Graphic abstract

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“…An example of such a drug is vinblastine, which binds to tubulin and blocks the formation of microtubules, thus inhibiting cell division [ 37 ]. It also shows a pro-apoptotic effect [ 9 , 38 , 39 ] and induces changes in the lysosomal compartment [ 40 , 41 ].…”

Section: Discussionmentioning

confidence: 99%

Emodin Sensitizes Cervical Cancer Cells to Vinblastine by Inducing Apoptosis and Mitotic Death

Trybus

Trybus²,

Król³

2022

IJMS

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In recent years, studies on the effects of combining novel plant compounds with cytostatics used in cancer therapy have received considerable attention. Since emodin sensitizes tumor cells to chemotherapeutics, we evaluated changes in cervical cancer cells after its combination with the antimitotic drug vinblastine. Cellular changes were demonstrated using optical, fluorescence, confocal and electron microscopy. Cell viability was assessed by MTT assay. The level of apoptosis, caspase 3/7, Bcl-2 protein, ROS, mitochondrial membrane depolarization, cell cycle and degree of DNA damage were analyzed by flow cytometry. The microscopic image showed indicators characteristic for emodin- and vinblastine-induced mitotic catastrophe, i.e., multinucleated cells, giant cells, cells with micronuclei, and abnormal mitotic figures. These compounds also increased blocking of cells in the G2/M phase, and the generated ROS induced swelling and mitochondrial damage. This translated into the growth of apoptotic cells with active caspase 3/7 and inactivation of Bcl-2 protein and active ATM kinase. Emodin potentiated the cytotoxic effect of vinblastine, increasing oxidative stress, mitotic catastrophe and apoptosis. Preliminary studies show that the combined action of both compounds, may constitute an interesting form of anticancer therapy.

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JNK and NFκB dependence of apoptosis induced by vinblastine in human acute promyelocytic leukaemia cells

Cited by 8 publications

References 25 publications

Curcumin-Induced Autophagy Augments Its Antitumor Effect against A172 Human Glioblastoma Cells

Curcumin-Induced Autophagy Augments Its Antitumor Effect against A172 Human Glioblastoma Cells

Naturally derived indole alkaloids targeting regulated cell death (RCD) for cancer therapy: from molecular mechanisms to potential therapeutic targets

Emodin Sensitizes Cervical Cancer Cells to Vinblastine by Inducing Apoptosis and Mitotic Death

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