Short-term treatment with glucosamine hydrochloride specifically downregulates hypoxia-inducible factor-1α at the protein level in YD-8 human tongue cancer cells

Jo, Jeong-Rang; Park, Yu-Kyoung; Jang, Byeong‐Churl

doi:10.3892/ijo.2014.2336

Cited by 7 publications

(6 citation statements)

References 42 publications

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“…Jung et al also reported that HIF‐1α was downregulated by glucosamine treatment in human oral cancer cells. Park et al reported similar results in prostate cancer cells . Therefore, HIF‐1 α suppression is a plausible GlcN antiallergic mechanism.…”

Section: Discussionmentioning

confidence: 68%

Glucosamine has an antiallergic effect in mice with allergic asthma and rhinitis

Jung

Kim

2017

Int Forum Allergy Rhinol

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Section: Discussionmentioning

confidence: 68%

Glucosamine has an antiallergic effect in mice with allergic asthma and rhinitis

Jung

Kim

2017

Int Forum Allergy Rhinol

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“…Hepatic cholesterol has been previously reported to activate HIF-1α, which may in turn damage the liver cells ( 31 ). Jo et al indicated that glucosamine hydrochloride may be used to treat oral tumors that demonstrate a high expression of HIF-1α, through reducing HIF-1α expression ( 32 ). Similar to the study by Jo et al ( 32 ), the Annexin V/PI staining data from the present study indicates that HIF-1α knockdown may promote the apoptosis of NCI-H157 cells ( Fig.…”

Section: Discussionmentioning

confidence: 99%

“…Jo et al indicated that glucosamine hydrochloride may be used to treat oral tumors that demonstrate a high expression of HIF-1α, through reducing HIF-1α expression ( 32 ). Similar to the study by Jo et al ( 32 ), the Annexin V/PI staining data from the present study indicates that HIF-1α knockdown may promote the apoptosis of NCI-H157 cells ( Fig. 2 ), which was the same effect that was caused by DDP.…”

Section: Discussionmentioning

confidence: 99%

Downregulation of HIF-1α inhibits the proliferation and invasion of non-small cell lung cancer NCI-H157 cells

Qian¹,

Bai²,

Gao³

et al. 2016

Oncology Letters

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Lung cancer, specifically non-small cell lung cancer (NSCLC), is the leading cause of cancer-associated mortality in the world. In previous years, almost no significant advancements have been made towards the molecular characterization of NSCLC, which highlights the requirement for novel target genes. Hypoxia inducible factor-1α (HIF-1α) is known to be essential in tumorigenesis, as it regulates the expression of numerous factors that are involved in angiogenesis, cellular proliferation and apoptosis. However, no direct association between HIF-1α and NSCLC treatment has previously been established. The aim of the present study was to characterize the effect of HIF-1α on NSCLC and to explore the possible mechanism. Additionally, HIF-1α small interfering (si)RNA and diamminedichloroplatinum (DDP) were used in combination to explore the combined effects on NSCLC cells. Lung carcinoma NCI-H157 cells were treated with HIF-1α small interfering (si)RNA, 5 µg/ml DDP or a combination of the two, and the proliferation, apoptosis and invasion ability of the cells were detected using a cell counting kit-8 assay, Annexin V/propidium iodide staining and a Transwell assay, respectively. In addition, the protein levels of caspase-3/9, anti-apoptotic protein B-cell lymphoma-2 (Bcl-2), vascular endothelial growth factor (VEGF), pigment epithelium-derived factor (PEDF), phosphoinositide 3-kinase (PI3K), phosphorylated (p-)PI3K, protein kinase B (AKT), p-AKT, extracellular signal-regulated kinase (ERK) and p-ERK were detected using western blot analysis. Similar to DPP treatment, HIF-1α siRNA treatment may reduce cell proliferation and the invasiveness of tumor cells while promoting apoptosis. Additionally, HIF-1α siRNA may increase the levels of the apoptotic proteins caspases 3 and 9 and inhibit the expression of Bcl-2. These anti-tumor effects may be acting through the VEGF/PEDF, PI3K/AKT and Raf/mitogen-activated protein kinase kinase/ERK signaling pathways. The effects of HIF-1α siRNA may be strengthened by DDP. The present data indicated that HIF-1α siRNA is important in the inhibition of NSCLC cells. Additionally, the effects of HIF-1α siRNA may be strengthened by DDP, which suggests that HIF-1α siRNA may be combined with DDP for the treatment of tumors.

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“…HIF‐1α is an angiogenic transcription factor 36 . The HIF‐1α expression is linked to the tumour promotion in human oral cancer 37 and correlates with the growth and adhesion in human OSCC cells 38,39 . In this study, we further determined whether HIF‐1α protein is expressed in YD‐38 cells and whether dasatinib modulates it.…”

Section: Resultsmentioning

confidence: 97%

Anti‐growth and pro‐apoptotic effects of dasatinib on human oral cancer cells through multi‐targeted mechanisms

Park

Yadav

et al. 2021

J Cellular Molecular Medi

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Dasatinib is an inhibitor of Src that has anti‐tumour effects on many haematological and solid cancers. However, the anti‐tumour effects of dasatinib on human oral cancers remain unclear. In this study, we investigated the effects of dasatinib on different types of human oral cancer cells: the non‐tumorigenic YD‐8 and YD‐38 and the tumorigenic YD‐10B and HSC‐3 cells. Strikingly, dasatinib at 10 µM strongly suppressed the growth and induced apoptosis of YD‐38 cells and inhibited the phosphorylation of Src, EGFR, STAT‐3, STAT‐5, PKB and ERK‐1/2. In contrast, knockdown of Src blocked the phosphorylation of EGFR, STAT‐5, PKB and ERK‐1/2, but not STAT‐3, in YD‐38 cells. Dasatinib induced activation of the intrinsic caspase pathway, which was inhibited by z‐VAD‐fmk, a pan‐caspase inhibitor. Dasatinib also decreased Mcl‐1 expression and S6 phosphorylation while increased GRP78 expression and eIF‐2α phosphorylation in YD‐38 cells. In addition, to its direct effects on YD‐38 cells, dasatinib also exhibited anti‐angiogenic properties. Dasatinib‐treated YD‐38 or HUVEC showed reduced HIF‐1α expression and stability. Dasatinib alone or conditioned media from dasatinib‐treated YD‐38 cells inhibited HUVEC tube formation on Matrigel without affecting HUVEC viability. Importantly, dasatinib's anti‐growth, anti‐angiogenic and pro‐apoptotic effects were additionally seen in tumorigenic HSC‐3 cells. Together, these results demonstrate that dasatinib has strong anti‐growth, anti‐angiogenic and pro‐apoptotic effects on human oral cancer cells, which are mediated through the regulation of multiple targets, including Src, EGFR, STAT‐3, STAT‐5, PKB, ERK‐1/2, S6, eIF‐2α, GRP78, caspase‐9/3, Mcl‐1 and HIF‐1α.

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Short-term treatment with glucosamine hydrochloride specifically downregulates hypoxia-inducible factor-1α at the protein level in YD-8 human tongue cancer cells

Cited by 7 publications

References 42 publications

Glucosamine has an antiallergic effect in mice with allergic asthma and rhinitis

Glucosamine has an antiallergic effect in mice with allergic asthma and rhinitis

Downregulation of HIF-1α inhibits the proliferation and invasion of non-small cell lung cancer NCI-H157 cells

Anti‐growth and pro‐apoptotic effects of dasatinib on human oral cancer cells through multi‐targeted mechanisms

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