Luteoloside Inhibits Proliferation of Human Chronic Myeloid Leukemia K562 Cells by Inducing G2/M Phase Cell Cycle Arrest and Apoptosis

Shao, Junli; Liang, Heng; Dai, Juanxiu

doi:10.4314/tjpr.v15i1.6

Cited by 3 publications

(2 citation statements)

References 27 publications

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“…On the other hand, luteoloside has a lesser effect on the growth of the normal cell HUVEC12 and LO2 at the tested concentrations ( Figure 1 B) with the IC 50 130.4 μM and 111.5 μM for 48 h treatment, respectively. In contrast, proliferation inhibition of luteoloside on several hepatocellular carcinoma cells [ 12 ], chronic myeloid leukemia cell K562 [ 29 ], colon carcinoma cell COLO 320 DM, and normal cell VERO [ 14 ] are also dose- and time-dependent with a IC 50 of approximately 100, 200, 266, and 854 μM, respectively, for 48 h treatment. Therefore, luteoloside may be a promising candidate for anti-cervical cancer agents with the advantages of high efficiency and low toxicity.…”

Section: Discussionmentioning

confidence: 99%

Luteoloside Inhibits Proliferation and Promotes Intrinsic and Extrinsic Pathway-Mediated Apoptosis Involving MAPK and mTOR Signaling Pathways in Human Cervical Cancer Cells

Shao

Wang

et al. 2018

IJMS

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Cervical cancer is a common gynecological malignancy with high incidence and mortality. Drugs commonly used in chemotherapy are often accompanied by strong side-effects. To find an anti-cervical cancer drug with high effects and low toxicity, luteoloside was used to treat the cervical cancer cell line Hela to investigate its effects on cell morphology, proliferation, apoptosis, and related proteins. The study demonstrated that luteoloside could inhibit proliferation remarkably; promote apoptosis and cytochrome C release; decrease the mitochondrial membrane potential and reactive oxygen species level; upregulate the expression of Fas, Bax, p53, phospho-p38, phospho-JNK, and cleaved PARP; downregulate the expression of Bcl-2 and phospho-mTOR; activate caspase-3 and caspase-8; change the nuclear morphology, and fragmentate DNA in Hela cells. These results strongly suggest that luteoloside can significantly inhibit the proliferation and trigger apoptosis in Hela cells. In contrast, luteoloside had less proliferation inhibiting effects on the normal cell lines HUVEC12 and LO2, and minor apoptosis promoting effects on HUVEC12 cells. Furthermore, the luteoloside-induced apoptosis in Hela cells is mediated by both intrinsic and extrinsic pathways and the effects of luteoloside may be regulated by the mitogen-activated protein kinases and mTOR signaling pathways via p53.

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Section: Discussionmentioning

confidence: 99%

Luteoloside Inhibits Proliferation and Promotes Intrinsic and Extrinsic Pathway-Mediated Apoptosis Involving MAPK and mTOR Signaling Pathways in Human Cervical Cancer Cells

Shao

Wang

et al. 2018

IJMS

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show abstract

“…The intensity of the antiproliferative effect of luteoloside in K562 cells followed a dose‐ and time‐dependent trend (IC 50 = 30.7 μM) with much less toxicity towards normal cells (IC 50 = 91.8 μM). Further, treatment with luteoloside downregulated cyclin B1 and resulted in G2/M phase arrest (Shao, Liang, & Dai, 2016). The crux from this study is that luteoloside‐provoked apoptosis is mediated by Bax and Bcl‐2 proteins and occurs through a mitochondrial pathway (Table 1).…”

Section: Luteolin In Anticancer Therapymentioning

confidence: 99%

Anticancer activity of the plant flavonoid luteolin against preclinical models of various cancers and insights on different signalling mechanisms modulated

Ganai

Sheikh

Baba

et al. 2021

Phytotherapy Research

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Various signaling mechanisms contribute significantly to the development of multiple cancers. Small molecules with the potential of influencing a wide variety of molecular targets may prove as broad-spectrum anticancer agents. Flavonoids from plant sources are strongly emerging as promising antineoplastic molecules because of their ability to hamper different cancer-driving signaling pathways. Further, these flavonoids offer an additional benefit due to their congenital antioxidant potential. This paper discusses the anticancer activity of luteolin against a number of cancers including leukemias, prostate cancer, pancreatic cancer, breast cancer, lung cancer, colorectal cancer, melanoma, liver, gastric, and brain cancer. Strong emphasis has been laid on key molecular mechanisms impacted by luteolin for exerting antineoplastic effect. Importantly, certain epigenetic targets like histone deacetylases (HDACs), DNA methylation regulator enzymes that are influenced by this befitting flavone for inducing cytotoxicity in certain preclinical cancer models, have also been made the part of this review. Additionally, the significantly improved therapeutic benefits of luteolin in combination with other therapeutics are comprehensively discussed. The current loopholes in luteolin research are also considered, which may open novel routes for further valuable studies on this promising flavone.

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Screening potential antileukemia agents from duckweed: Integration of chemical profiling, network pharmacology, and experimental validation

Liu,

Huang,

Yang

et al. 2024

Phytochemical Analysis

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IntroductionThe identification of active dietary flavonoids in food is promising for novel drug discovery. The active ingredients of duckweed (a widely recognized food and herb with abundant flavonoids) that are associated with acute myeloid leukemia (AML) have yet to be identified, and their underlying mechanisms have not been elucidated.ObjectivesThe objective of this study was to identify novel constituents exhibiting antileukemia activity in duckweed through the integration of chemical profiling, network pharmacology, and experimental validation.MethodsFirst, high performance liquid chromatography‐tandem mass spectrometry (HPLC‐MS/MS) was used to characterize the primary constituents of duckweed. Subsequently, AML cell‐xenograft tumor models were used to validate the anticancer effect of duckweed extract. Furthermore, network pharmacology analysis was conducted to predict the potential active compounds and drug targets against AML. Lastly, based on these findings, two monomers (apiin and luteoloside) were selected for experimental validation.ResultsA total of 17 compounds, all of which are apigenin and luteolin derivatives, were identified in duckweed. The duckweed extract significantly inhibited AML cell growth in vivo. Furthermore, a total of 88 targets for duckweed against AML were predicted, with key targets including PTGS2, MYC, MDM2, VEGFA, CTNNB1, CASP3, EGFR, TP53, HSP90AA1, CCND1, MMP9, TNF, and MAPK1. GO and KEGG pathway enrichment analyses indicated that these targets were primarily involved in the apoptotic signaling pathway. Lastly, both apiin and luteoloside effectively induced apoptosis through CASP3 activation, and this effect could be partially reversed by a caspase inhibitor (Z‐VAD).ConclusionDuckweed extract has an antileukemic effect, and apiin derived from duckweed shows potential as a treatment for AML.

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Luteoloside Inhibits Proliferation of Human Chronic Myeloid Leukemia K562 Cells by Inducing G2/M Phase Cell Cycle Arrest and Apoptosis

Cited by 3 publications

References 27 publications

Luteoloside Inhibits Proliferation and Promotes Intrinsic and Extrinsic Pathway-Mediated Apoptosis Involving MAPK and mTOR Signaling Pathways in Human Cervical Cancer Cells

Luteoloside Inhibits Proliferation and Promotes Intrinsic and Extrinsic Pathway-Mediated Apoptosis Involving MAPK and mTOR Signaling Pathways in Human Cervical Cancer Cells

Anticancer activity of the plant flavonoid luteolin against preclinical models of various cancers and insights on different signalling mechanisms modulated

Screening potential antileukemia agents from duckweed: Integration of chemical profiling, network pharmacology, and experimental validation

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