scholarly journals Vitamin D inhibits the proliferation of Oral Squamous Cell Carcinoma by suppressing lncRNA LUCAT1 through the MAPK pathway

2020 ◽  
Vol 11 (20) ◽  
pp. 5971-5981
Author(s):  
Tingting Jin ◽  
Yin Guo ◽  
Zixian Huang ◽  
Qianyu Zhang ◽  
Zhuoshan Huang ◽  
...  
Keyword(s):  
Vitamin D ◽  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Mapk Pathway

scholarly journals Noncalcemic Vitamin D Hydroxyderivatives Inhibit Human Oral Squamous Cell Carcinoma and Down-regulate Hedgehog and WNT/β-Catenin Pathways

2020 ◽  
Vol 40 (5) ◽  
pp. 2467-2474 ◽  
Author(s):  
ALLEN S.W. OAK ◽  
GEORGETA BOCHEVA ◽  
TAE-KANG KIM ◽  
ANNA A. BROŻYNA ◽  
ZORICA JANJETOVIC ◽  
...  
Keyword(s):  
Vitamin D ◽  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell

scholarly journals Serum levels of 25‐hydroxy‐vitamin D in patients with oral squamous cell carcinoma: Making a case for chemoprevention

2020 ◽  
Vol 6 (4) ◽  
pp. 428-432
Author(s):  
Samuel E. Udeabor ◽  
Abdullah M. Albejadi ◽  
Waleed A. K. Al‐Shehri ◽  
Chidozie I. Onwuka ◽  
Saeed Y. Al‐Fathani ◽  
...  
Keyword(s):  
Vitamin D ◽  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Serum Levels ◽  
25 Hydroxy Vitamin D

scholarly journals MiR-148a inhibits oral squamous cell carcinoma progression through ERK/MAPK pathway via targeting IGF-IR

2020 ◽  
Vol 40 (4) ◽  
Author(s):  
Tingting Jia ◽  
Yipeng Ren ◽  
Fengze Wang ◽  
Rui Zhao ◽  
Bo Qiao ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Mapk Pathway ◽  
Mapk Signaling ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Node Metastasis ◽  
Erk Mapk

Abstract Objective: The current study aimed to investigate the functional roles and clinical significance of microRNA-148a (miR-148a) in the progression of oral squamous cell carcinoma (OSCC). Methods: Relative expression of miR-148a in OSCC cells and tissues were detected using quantitative real-time polymerase chain reaction (qRT-PCR). Chi-square test was performed to estimate the relationship between miR-148a expression and clinical characteristics of OSCC patients. Cell transfection was carried out using Lipofectamine® 2000. Biological behaviors of tumor cells were detected using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and transwell assays. Bioinformatics analysis and luciferase reporter assay were used to identify the target genes of miR-148a. Protein expression was detected through Western blot analysis. Results: MiR-148a expression was obviously decreased in OSCC tissues and cells, and such down-regulation was closely correlated with lymph node metastasis (P=0.027) and tumor node metastasis (TNM) stage (P=0.001) of OSCC patients. miR-148a overexpression could significantly impair OSCC cell proliferation, migration and invasion in vitro (P<0.05 for all). Insulin-like growth factor-I receptor (IGF-IR) was a potential target of miR-148a. MiR-148a could inhibit ERK/MAPK signaling pathway through targeting IGF-IR. Conclusion: MiR-148a plays an anti-tumor role in OSCC and inhibits OSCC progression through suppressing ERK/MAPK pathway via targeting IGF-IR.

scholarly journals Vitamin D promotes the cisplatin sensitivity of oral squamous cell carcinoma by inhibiting LCN2-modulated NF-κB pathway activation through RPS3

2019 ◽  
Vol 10 (12) ◽  
Author(s):  
Zixian Huang ◽  
Yin Zhang ◽  
Haigang Li ◽  
Yufeng Zhou ◽  
Qianyu Zhang ◽  
...  
Keyword(s):  
Vitamin D ◽  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Cancer Progression ◽  
Squamous Cell ◽  
Cisplatin Resistance ◽  
Biomedical Science ◽  
Lipocalin 2

AbstractChemoresistance is a major cause of cancer progression and the mortality of cancer patients. Developing a safe strategy for enhancing chemosensitivity is a challenge for biomedical science. Recent studies have suggested that vitamin D supplementation may decrease the risk of many cancers. However, the role of vitamin D in chemotherapy remains unknown. We found that vitamin D sensitised oral cancer cells to cisplatin and partially reversed cisplatin resistance. Using RNA-seq, we discovered that lipocalin 2 (LCN2) is an important mediator. Cisplatin enhanced the expression of LCN2 by decreasing methylation at the promoter, whereas vitamin D enhanced methylation and thereby inhibited the expression of LCN2. Overexpression of LCN2 increased cell survival and cisplatin resistance both in vitro and in vivo. High LCN2 expression was positively associated with differentiation, lymph node metastasis, and T staging and predicted a poor prognosis in oral squamous cell carcinoma (OSCC) patients. LCN2 was also associated with post-chemotherapy recurrence. Moreover, we found that LCN2 promoted the activation of NF-κB by binding to ribosomal protein S3 (RPS3) and enhanced the interaction between RPS3 and p65. Our study reveals that vitamin D can enhance cisplatin chemotherapy and suggests that vitamin D should be supplied during chemotherapy; however, more follow-up clinical studies are needed.

scholarly journals The Effects of 5-fluorouracil Alone and in Combination with 13-cis Retinoic Acid and Vitamin D3 on Human Oral Squamous Cell Carcinoma Lines

2012 ◽  
Vol 13 (3) ◽  
pp. 345-350 ◽  
Author(s):  
Zohreh Dalirsani ◽  
Safar Farajnia ◽  
Yousef Javadzadeh ◽  
Masoumeh Mehdipour ◽  
Sepideh Koozegari
Keyword(s):  
Vitamin D ◽  
Cell Proliferation ◽  
Squamous Cell Carcinoma ◽  
Retinoic Acid ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Inhibitory Effect ◽  
Apoptotic Effect ◽  
Advanced Stages

ABSTRACT Aim Oral squamous cell carcinoma (OSCC) is responsible for about 90% of oral malignancies and its incidence is increasing. Despite various treatment protocols, survival rate of OSCC is low. Chemotherapy that is used for treating this carcinoma in advanced stages is systemic therapy that destroys carcinogenic cells, and controls tumor metastasis. Chemotherapy is very toxic and has limitations, especially for patients in advanced stages. Considering positive effects of retinoid and vitamin D3 derivatives in treating some carcinomas, we decided to evaluate the effect of combination of these drugs on OSCC. In this study the effects of combination of 5-fluorouracil, 13-cis retinoic acid and vitamin D3 on cultured cell of OSCC have been evaluated. Materials and methods OSCC cells were cultured in culture media and different concentration of 5-fluorouracil, 13-cis retinoic acid and vitamin D3 were added to cultured cell as separately and in combinations. The effect of treatment on cell proliferation and induction of apoptosis were evaluated by MTT and TUNEL assays respectively. Results Combination of 5-fluorouracil and 13- cis retinoic acid had the highest inhibitory effect on SCC cell proliferation. Combination of two drugs had more apoptotic effect than each of them separately, and combination of three drugs had more effect than combination of two drugs. Conclusion Because combination of drugs had more inhibitory effect on cell proliferation than one of them and combination of three drugs had the most apoptotic effect than one of these drugs separately, these drugs may have synergic effect on OSCC. Clinical significance Combination of three drugs has more inhibitory effect on cell proliferation and apoptotic effect than one of these drugs. How to cite this article Dalirsani Z, Farajnia S, Javadzadeh Y, Mehdipour M, Koozegari S. The Effects of 5-fluorouracil Alone and in Combination with 13-cis Retinoic Acid and Vitamin D3 on Human Oral Squamous Cell Carcinoma Lines. J Contemp Dent Pract 2012;13(3):345-350.

scholarly journals Contribution of p38 MAPK Pathway to Norcantharidin-Induced Programmed Cell Death in Human Oral Squamous Cell Carcinoma

2019 ◽  
Vol 20 (14) ◽  
pp. 3487 ◽  
Author(s):  
Chi-Hyun Ahn ◽  
Kyoung-Ok Hong ◽  
Bohwan Jin ◽  
WonWoo Lee ◽  
Yun Chan Jung ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Death ◽  
Oral Squamous Cell Carcinoma ◽  
Programmed Cell Death ◽  
Cell Carcinoma ◽  
P38 Mapk ◽  
Cell Lines ◽  
Squamous Cell ◽  
Mapk Pathway ◽  
Terminal Deoxynucleotidyl Transferase

Norcantharidin (NCTD), a demethylated analog of cantharidin isolated from blister beetles, has been used as a promising anticancer agent; however, the underlying function of NCTD against human oral squamous cell carcinoma (OSCC) has not been fully understood. Here, this study was aimed to investigate the apoptotic effect and molecular targets of NCTD in human OSCC in vitro and in vivo. The anticancer effects of NCTD and its related molecular mechanisms were evaluated by trypan blue exclusion assay, live/dead assay, western blotting, 4-6-Diamidino-2-Phenylindole (DAPI) staining, flow cytometric analysis, Terminal Deoxynucleotidyl Transferase dUTP Nick end Labeling (TUNEL) assay, and immunohistochemistry. NCTD significantly inhibited cell growth and increased the number of dead cells in HSC-3 and HN22 cell lines. It induced the following apoptotic phenomena: (1) the cleavages of poly (ADP-ribose) polymerase and casepase-3; (2) increase in apoptotic morphological changes (nuclear condensation and fragmentation); (3) increase in annexin V-positive cells or sub-G1 population of cells. NCTD significantly activated the p38 mitogen-activated protein kinase (MAPK) pathway but inactivated the signal transducer and activator of transcription (STAT)3 pathway. A p38 MAPK inhibitor (SB203580) partially attenuated NCTD-induced programmed cell death (apoptosis) in both cell lines, whereas ectopic overexpression of STAT3 did not affect it. NCTD strongly suppressed tumor growth in the tumor xenograft bearing HSC-3 cells, and the number of TUNEL-positive cells increased in NCTD-treated tumor tissues. In addition, NCTD did not cause any histopathological changes in the liver nor the kidney. NCTD induced programmed cell death via the activation of p38 MAPK in OSCC. Therefore, these results suggest that NCTD could be a potential anticancer drug candidate for the treatment of OSCC.

scholarly journals In serum, higher parathyroid hormone but not lower vitamin D is associated with oral squamous cell carcinoma

2015 ◽  
Vol 22 (4) ◽  
pp. 259 ◽  
Author(s):  
H. Zhang ◽  
H. Lu ◽  
C. Shrestha ◽  
Y. Feng ◽  
Y. Li ◽  
...  
Keyword(s):  
Vitamin D ◽  
Squamous Cell Carcinoma ◽  
Parathyroid Hormone ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Serum Vitamin ◽  
Serum Vitamin D ◽  
Differentiation And Proliferation ◽  
Serum Pth

IntroductionVitamin D and calcium are known to regulate differentiation and proliferation of keratinocytes; they might potentially have a role in suppressing carcinogenesis in squamous epithelium. Serum parathyroid hormone (pth) is a sensitive indicator of calcium and vitamin D deficiency, and 25-hydroxyvitamin D [25(OH)D] is an established marker of vitamin D status.MethodsTo determine whether levels of 25(OH)D, calcium, or pth in serum are associated with oral squamous cell carcinoma (oscc), we examined those parameters in serum collected from 70 patients with oscc and from an equal number of matched control subjects.ResultsThe results showed that intact pth was significantly higher in serum from oscc patients than in serum from control subjects. However, we observed no significant differences in 25(OH)D or calcium in serum from oscc patients and from control subjects.ConclusionsWe conclude that higher serum pth, but not lower serum vitamin D or calcium, is associated with oscc.

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