Curcumin and tetrahydrocurcumin induce cell death in Ara-C-resistant acute myeloid leukemia.
The results demonstrated that curcumin and tetrahydrocurcumin induced cell death by apoptosis and autophagy, respectively, in Ara-C-resistant HL60 cells.
Leukemia · LIVING RESEARCH LIBRARY
Ongoing Research for Leukemia Using Advanced Alternative Medicine
Explore positive published findings by substance, cancer biology, treatment interaction and quality-of-life outcome.
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Research organized by substance and finding
Browse 20 source-linked studies with the full title, publication year, research focus and a concise finding. Select any linked substance to move directly to its corresponding Sunridge page.
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Curcumin attenuates Adriamycin-resistance of acute myeloid leukemia by inhibiting the lncRNA HOTAIR/miR-20a-5p/WT1 axis.
Furthermore, curcumin suppressed proliferation and promoted apoptosis of HL-60/ADR cells.
Curcumin augments therapeutic efficacy of TRAIL-based immunotoxins in leukemia.
Overall, our results suggest that curcumin potentiates TRAIL-induced apoptosis through modulation of death receptors and anti-apoptotic proteins which significantly enhances the therapeutic efficacy.
Curcumin sensitizes response to cytarabine in acute myeloid leukemia by regulating intestinal microbiota.
Curcumin treatment sensitized response to Ara-C in MNCs of AML mice, but had no direct effect on AML cell lines.
(-)-Epigallocatechin-3-gallate induces apoptosis and differentiation in leukaemia by targeting reactive oxygen species and PIN1.
Moreover, EGCG showed inhibition of ROS production in NB4 cells in the presence of N-acetyl-L-cysteine (NAC), as well as a partial blockage of neutrophil differentiation and apoptosis, indicating that EGCG-activities involve/or are in response of oxidative stress.
Self-Assembled Daunorubicin/Epigallocatechin Gallate Nanocomplex for Synergistic Reversal of Chemoresistance in Leukemia.
Epigallocatechin gallate (EGCG), a bioactive polyphenol from green tea, has attracted immense interest as a potential chemosensitizer, but its application is limited due to the need for effective formulations capable of co-delivering EGCG and anti-leukemic drugs.
SphK1 inhibitor potentiates the anti-cancer effect of EGCG on leukaemia cells.
The study reports sphK1 inhibitor potentiates the anti-cancer effect of EGCG on leukaemia cells.
Ginsenoside 24-OH-PD from red ginseng inhibits acute T-lymphocytic leukaemia by activating the mitochondrial pathway.
Ginsenoside 24-hydroxy-ginsengdiol (24-OH-PD), extracted from red ginseng, is a novel diol-type ginsenoside, strongly inhibits the growth of human T-cell acute lymphoblastic leukaemia (T-ALL) CCRF-CEM cells.
Essential functions of inositol hexakisphosphate (IP6) in murine leukemia virus replication.
Interestingly, we discovered a key difference in the role of IP6 in MLV versus HIV-1: while HIV-1 is not dependent upon IP6 levels in target cells, MLV replication is significantly reduced in IP6-deficient cell lines.
Melatonin inhibits MLL-rearranged leukemia via RBFOX3/hTERT and NF-κB/COX-2 signaling pathways.
In this study, melatonin inhibited cell proliferation and induced apoptosis by activating the caspase-dependent apoptotic pathway in MLL-r leukemia cells.
Multitarget effects of quercetin in leukemia.
Furthermore, in vivo administration of quercetin significantly reduced tumor volume in P39 xenografts and confirmed in vitro results regarding apoptosis, autophagy, and cell-cycle arrest.
Quercetin inhibits the cAMP/PKA/CREB/glycolysis axis to exert anti-acute lymphoblastic leukemia effects.
Quercetin (Que) demonstrates broad antitumor effects by inhibiting glycolysis and cell proliferation.
Rapamycin increases leukemia cell sensitivity to chemotherapy by regulating mTORC1 pathway-mediated apoptosis and autophagy.
Analysis by cell counting kit-8, western blot, flow cytometry, and immunohistochemistry was performed, and results suggested that both rapamycin and chemotherapy inhibited proliferation of SHI-1 cells both in vitro and in vivo, suppressed neoplasm growth in vivo, and promoted survival of NPG AML mice.
Rapamycin induces human acute promyelocytic leukemia cell HL-60 autophagic apoptosis.
HL-60 cell proliferation could be significantly inhibited by rapamycin (80 μg/mL-640 μg/mL), which was in a dose-dependent manner.
Rapamycin inhibits the progression of human acute myeloid leukemia by regulating the circ_0094100/miR-217/ATP1B1 axis.
Rapamycin treatment suppressed AML cell viability and promoted apoptosis in a dose-dependent way.
Involvement of Sphingolipid Metabolism Enzymes in Resveratrol-Mediated Cytotoxicity in Philadelphia-Positive Acute Lymphoblastic Leukemia.
The anti-proliferative and apoptotic effects of resveratrol alone and in combination with SPT inhibitor (myriocin), SK inhibitor (SKI II), GCS inhibitor (PDMP) were determined by MTT cell proliferation assay and flow cytometry, respectively.
Antitumor effects of sodium selenite on acute lymphocytic leukemia.
We trialed the different dosages (0 × 106 M, 2.7 × 106 M, 5.4 × 106 M, and 8.1 × 106 M) of sodium selenite given to the acute lymphocytic leukemia cell lines incubated for 24, 48, and 72 h.
Cytosolic JNK-dependent microtubule reassembly protects Jurkat leukemia cells from selenite-induced apoptosis.
It has been shown that selenite inhibits tumor growth through regulation of microtubule dynamics, however, the exact underlying mechanisms remained to be fully elucidated.
Retinoic acid and ascorbate synergize to suppress myeloid leukemia via TET2 activation.
Using Tet1/2/3-deficient mice and primary human acute myeloid leukemia (AML) models, we show that ATRA plus ascorbate more effectively induces differentiation, inhibits leukemia stem cell self-renewal in a TET2-dependent manner, and sensitizes AML cells to targeted therapies in vivo, leading to improved survival.
Vitamin D decreases STAT phosphorylation and inflammatory cytokine output in T-LGL leukemia.
Doses of 10 and 100 nM calcitriol also significantly decreased the inflammatory cytokine IFN-γ in the TL-1 cell line.
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