Effects of d-allose in combination with docetaxel in human head and neck cancer cells

Indo, Kanako; Hoshikawa, Hiroshi; Kamitori, Kazuyo; Yamaguchi, Fuminori; Mori, Terusige; Tokuda, Masaaki; Mori, Nozomu

doi:10.3892/ijo.2014.2590

Cited by 27 publications

(22 citation statements)

References 33 publications

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“…DTX is widely used as a cancer treatment (6)(7)(8)(9)(10)(11)(12)(13)(14). However, the emergence of chemotherapeutic resistance iTHs universal and DTX-resistance responses have been observed in a number of patients (15).…”

Section: Discussionmentioning

confidence: 99%

“…Docetaxel (DTX) is a well-established anti-mitotic chemotherapy agent that functions by interfering with cell division (5). It is used to treat a number of cancer types including metastatic or advanced breast, prostate, thyroid, gastric, ovarian and lung cancer based on its pro-apoptosis potential and its inhibitory effect on angiogenesis and cell viability (6)(7)(8)(9)(10)(11)(12)(13)(14). DTX has also been demonstrated to upregulate growth/differentiation factor 15 and results in chemoresistance in prostate cancer (15).…”

Section: Introductionmentioning

confidence: 99%

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CCL2 influences the sensitivity of lung cancer A549 cells to docetaxel

et al. 2018

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Abstract. Lung cancer is one of the most common malignant tumor types globally. Acquisition of chemoresistance in lung cancer cells is the primary cause of chemotherapy failure. Inflammatory chemokine C-C motif chemokine ligand 2 (CCL2) has been reported to be involved in the progression of cancer and drug resistance. However, its function in docetaxel (DTX) resistance of lung cancer remains unclear. In the present study, the mechanism underlying DTX-induced drug resistance was investigated. Reverse transcription-quantitative polymerase chain reaction and western blot analysis revealed that DTX treatment increased the mRNA and protein expression of CCL2 in lung cancer A549 cells. CCL2 was knocked down by small interfering RNA or was overexpressed by recombinant CCL2 lentivirus, and cell viability was determined. An MTT assay indicated that CCL2 downregulation decreased the viability of A549 cells and augmented the DTX-induced cytotoxicity, whereas CCL2 upregulation protected A549 cells from DTX-induced cytotoxicity. Additionally, it was revealed that CCL2 overexpression activated phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) signaling and inhibited apoptosis-associated protein caspase-3 activation and B-cell lymphoma 2 (Bcl-2) phosphorylation at Ser 70 induced by DTX, and enhanced DTX-induced Bcl-2-associated death promoter phosphorylation at Ser 112 . PI3K/AKT inhibitor LY294002 restored DTX-induced caspase-3 activation and Bcl-2 phosphorylation, reversed the effect of CCL2 on the viability of A549 cells and enhanced DTX-induced cytotoxicity. These results demonstrated that chemoresistance may be mediated by cell stress responses involving CCL2 expression, suggesting that CCL2 may be a potential target for enhancing the therapeutic effect of DTX in lung cancer.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

CCL2 influences the sensitivity of lung cancer A549 cells to docetaxel

et al. 2018

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“…Notably, TXNIP deficiency initiated hepatocellular carcinogenesis in transgenic mice (20). In addition, recent reports have shown that D-allose stimulates the expression of TXNIP in several kinds of malignancy (7,9,21,22).…”

Section: Introductionmentioning

confidence: 99%

“…Recent studies have shown that D-allose has growth inhibitory effects in several kinds of malignancies including hepatocellular carcinoma, prostate, ovarian, and head and neck cancers, and leukaemia (3)(4)(5)(6)(7)(8)(9). However, the effect of D-allose on lung cancer progression has not been studied.…”

Section: Introductionmentioning

confidence: 99%

Additive antitumour effect of D‑allose in combination with cisplatin in non-small cell lung cancer cells

et al. 2018

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D‑allose is a rare sugar which has been shown to have growth inhibitory effects in several kinds of malignancies. However, the effect of D‑allose on lung cancer progression has not been previously studied. To investigate the antitumour effect of D‑allose in lung cancer cells and its mechanism, human non-small cell lung cancer (NSCLC) cell lines (squamous cell carcinomas: EBC1 and VMRC‑LCD; adenocarcinomas: A549, HI1017, RERF‑LC‑A1 and NCI-H1975) were treated with D‑allose (50 mM) with or without cisplatin (5 µM). D‑allose inhibited cell growth, particularly in EBC1 and VMRC‑LCD cells. In combination with cisplatin, D‑allose had a synergistic growth inhibitory effect. D‑allose increased the expression of thioredoxin interacting protein (TXNIP) at mRNA and protein levels. D‑allose decreased the proportion of cells in G1 phase and increased those in S and G2/M phases. For in vivo experiments, EBC1 cells were inoculated into BALB/c-nu mice. After tumourigenesis, D‑allose and cisplatin were injected. In this mouse xenograft model, additional treatment with D‑allose showed a significantly greater tumour inhibitory effect compared with cisplatin alone, accompanied by lower Ki‑67 and higher TXNIP expression. In conclusion, D‑allose inhibited NSCLC cell proliferation in vitro and tumour progression in vivo. In combination with cisplatin, D‑allose had an additional antitumour effect. Specifically, increased TXNIP expression and subsequent G2/M arrest play a role in D‑allose-mediated antitumour effects in NSCLC.

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“…Although D-allose is particularly rare in nature, in addition to its general characteristics of rare sugars, it also has important physiological activities such as lowering blood lipid and blood sugar concentration, reducing free radicals and improving intestinal flora (Gao et al 2011). Studies have found that D-allose can induce programmed cell apoptosis in malignant tumor cells, reduce the production of oxygen free radicals in inflammatory reaction and inhibit leukocyte activation, exerting its anti-inflammatory effects to protect liver, kidney and retina from I/R injury (Mizote et al 2011;Indo et al 2014;Liu et al 2014).…”

Section: Introductionmentioning

confidence: 99%

D-allose alleviates ischemia/reperfusion (I/R) injury in skin flap via MKP-1

Hou

Zhang

2020

Mol Med

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Background: D-allose was promising in the protection of ischemia/reperfusion (I/R) injury. We intended to investigate the function of D-allose in skin flap of rat followed by the injury of I/R and whether ERK signal pathway was involved in. Methods: The back flap of Wistar rats was picked up with a vascular bundle of the lateral chest wall. I/R model was made by the venous clamp for 6 h. Rats received D-allose and PD-98059, the inhibitor of ERK1/2, 30 min before modeling. Morphology of tissue was observed by HE staining. Nitric oxide (NO), myeloperoxidase (MPO), malondialdehyde (MDA) and superoxide dismutase (SOD) levels in skin flap were determined by ELISA kits. mRNA and protein levels were determined by qPCR and Western blot respectively. Results: D-allose alleviated the condition of pathological changes and raised the survival rate of skin flap injured by I/R. Moreover, D-allose suppressed NO, MPO and MDA while elevated SOD levels during I/R status. Furthermore, Dallose decreased MCP-1, TNF-α, IL-1β and IL-6 levels in skin flap injured by I/R. In addition, D-allose inhibited MKP-1 expression and activated ERK1/2 pathway in skin flap injured by I/R. PD-98059 partially counteracted D-allose effects on I/R injury. Conclusions: D-allose exerted its protective function via inhibiting MKP-1expression and further activated ERK1/2 pathway to suppress the progress of oxidative stress, inflammation and necrosis, contributing to the survival of skin flap injured by I/R. Thus, D-allose was promising in the transplantation of skin flap.

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Effects of d-allose in combination with docetaxel in human head and neck cancer cells

Cited by 27 publications

References 33 publications

CCL2 influences the sensitivity of lung cancer A549 cells to docetaxel

CCL2 influences the sensitivity of lung cancer A549 cells to docetaxel

Additive antitumour effect of D‑allose in combination with cisplatin in non-small cell lung cancer cells

D-allose alleviates ischemia/reperfusion (I/R) injury in skin flap via MKP-1

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