Design, synthesis and antimetastatic evaluation of 1-benzothiazolylphenylbenzotriazoles for photodynamic therapy in oral cancer cells

MedChemComm ◽  
2016 ◽  
Vol 7 (6) ◽  
pp. 1151-1158 ◽  
Author(s):  
Gopal Chandru Senadi ◽  
Chieh-Ming Liao ◽  
Kung-Kai Kuo ◽  
Jian-Cheng Lin ◽  
Long-Sen Chang ◽  
...  

We have designed and synthesized a new series of 1-benzothiazolylphenylbenzotriazoles 9a–p and studied their antimetastatic mechanism involved in photosensitive effects induced by UVA in oral cancer cell Ca9-22.

2016 ◽  
Vol 15 (04) ◽  
pp. 1650015 ◽  
Author(s):  
G. Jocelin ◽  
A. Arivarasan ◽  
M. Ganesan ◽  
N. Rajendra Prasad ◽  
G. Sasikala

Quantum dots (QDs) are gaining widespread recognition for its luminescence behavior and unique photo physical properties as a bio-marker and inorganic fluorophore. In spite of such rampant advantages, its application is clinically hampered depending on the surface coating decreasing its luminescence efficiency. The present study reports preparation of CdTe QDs capped with biologically active thiol based material, mercaptosuccinic acid (MSA) for diagnosis of oral cancer (KB) cells by acting as a fluorophore marking targeted tumor cells and at the same time exhibiting certain cytotoxic effects. Synthesized MSA coated CdTe QDs is spherical in shape with an average particle size of 3–5[Formula: see text]nm. In vitro, the rapid uptake of MSA CdTe QDs in oral cancer cell lines were assessed through fluorescence microscopy. Further, this study evaluates the therapeutic efficiency of MSA CdTe QDs in human oral cancer cell lines using MTT analysis. MSA CdTe QDs exhibit significant cytotoxicity in oral cancer cells in a dose dependent manner with low IC50 when compared with other raw CdTe QDs. MSA CdTe QDs were also treated with human lymphocytes (normal cells) to assess and compare the toxicity profile of QDs in normal and oral tumors. The results of our present study strengthen our hypothesis of using MSA CdTe QDs as detector for tracking and fluorescence imaging of oral cancer cells and exhibiting sufficient cytotoxicity in them.


2021 ◽  
Vol 22 (16) ◽  
pp. 8686
Author(s):  
Rajdeep Chakraborty ◽  
Karen Vickery ◽  
Charbel Darido ◽  
Shoba Ranganathan ◽  
Honghua Hu

Oral cancer is a major global health problem with high incidence and low survival rates. The oral cavity contains biofilms as dental plaques that harbour both Gram-negative and Gram-positive bacterial antigens, lipopolysaccharide (LPS) and lipoteichoic acid (LTA), respectively. LPS and LTA are known to stimulate cancer cell growth, and the bioactive phytochemical capsaicin has been reported to reverse this effect. Here, we tested the efficacy of oral cancer chemotherapy treatment with capsaicin in the presence of LPS, LTA or the combination of both antigens. LPS and LTA were administered to Cal 27 oral cancer cells prior to and/or concurrently with capsaicin, and the treatment efficacy was evaluated by measuring cell proliferation and apoptotic cell death. We found that while capsaicin inhibits oral cancer cell proliferation and metabolism (MT Glo assay) and increases cell death (Trypan blue exclusion assay and Caspase 3/7 expression), its anti-cancer effect was significantly reduced on cells that are either primed or exposed to the bacterial antigens. Capsaicin treatment significantly increased oral cancer cells’ suppressor of cytokine signalling 3 gene expression. This increase was reversed in the presence of bacterial antigens during treatment. Our data establish a rationale for clinical consideration of bacterial antigens that may interfere with the treatment efficacy of oral cancer.


Author(s):  
Nenavath Vinay ◽  
Darling Chellathai David

Background: Cancer is rapidly evolving life-threatening ailment in the mankind due to changes in daily food intake and lifestyle changes. Oral carcinoma is 6th major cause of cancer death in the world and it is third major reason of cancer mortality in India. Every cell in the human body requires glucose for its metabolic energy. Besides normal cell, cancer cells also require the glucose for its endurance and multiplication. SGLT2 inhibitors which are aimed at diabetes therapy exhibited anticancer properties also in colon and pancreatic cancer lines. Present study aim is to evaluate the anticancer activity of SGLT2 inhibitors against oral cancer cell by MTT Assay.Methods: To evaluate the anticancer activity of SGLT2 inhibitors MTT Cytotoxic assay is performed as per standard protocols. Cancer cells were plated in 24-well plates and incubated at 370C with 5% CO2 condition. After convergence, samples are added to the plates in various concentrations and allowed to incubate then they are detached from the plates and cleansed with the reagents. The wells are coated with the dye and incubated. Later samples are analysed in UV-spectrophotometer.Results: Cytotoxic assay showed decrease in cell viability with increasing dose of SGLT2 inhibitors. IC50 values were determined graphically. The IC50 value of dapagliflozin is 400µg/ml and canagliflozin is 250µg/ml respectively after 24 hours of Assessment.Conclusions: The results of the current study give us an evidence that SGLT2 inhibitors dapagliflozin and canagliflozin exhibits anticancer property in Oral Cancer cell line.


2021 ◽  
Vol 14 (10) ◽  
pp. 994
Author(s):  
Kun-Han Yang ◽  
Yu-Sheng Lin ◽  
Sheng-Chieh Wang ◽  
Min-Yu Lee ◽  
Jen-Yang Tang ◽  
...  

Dihydrosinularin (DHS) is an analog of soft coral-derived sinularin; however, the anticancer effects and mechanisms of DHS have seldom been reported. This investigation examined the antiproliferation ability and mechanisms of DHS on oral cancer cells. In a cell viability assay, DHS showed growth inhibition against several types of oral cancer cell lines (Ca9-22, SCC-9, OECM-1, CAL 27, OC-2, and HSC-3) with no cytotoxic side effects on non-malignant oral cells (HGF-1). Ca9-22 and SCC-9 cell lines showing high susceptibility to DHS were selected to explore the antiproliferation mechanisms of DHS. DHS also causes apoptosis as detected by annexin V, pancaspase, and caspase 3 activation. DHS induces oxidative stress, leading to the generation of reactive oxygen species (ROS)/mitochondrial superoxide (MitoSOX) and mitochondrial membrane potential (MitoMP) depletion. DHS also induced DNA damage by probing γH2AX phosphorylation. Pretreatment with the ROS scavenger N-acetylcysteine (NAC) can partly counter these DHS-induced changes. We report that the marine natural product DHS can inhibit the cell growth of oral cancer cells. Exploring the mechanisms of this cancer cell growth inhibition, we demonstrate the prominent role DHS plays in oxidative stress.


Biomolecules ◽  
2020 ◽  
Vol 10 (5) ◽  
pp. 777 ◽  
Author(s):  
Tzu-Jung Yu ◽  
Jen-Yang Tang ◽  
Fu Ou-Yang ◽  
Yen-Yun Wang ◽  
Shyng-Shiou F. Yuan ◽  
...  

Withaferin A (WFA) has been reported to inhibit cancer cell proliferation based on high cytotoxic concentrations. However, the low cytotoxic effect of WFA in regulating cancer cell migration is rarely investigated. The purpose of this study is to investigate the changes in migration and mechanisms of oral cancer Ca9-22 cells after low concentrations of WFA treatment. WFA under 0.5 μM at 24 h treatment shows no cytotoxicity to oral cancer Ca9-22 cells (~95% viability). Under this condition, WFA triggers reactive oxygen species (ROS) production and inhibits 2D (wound healing) and 3D cell migration (transwell) and Matrigel invasion. Mechanically, WFA inhibits matrix metalloproteinase (MMP)-2 and MMP-9 activities but induces mRNA expression for a group of antioxidant genes, such as nuclear factor, erythroid 2-like 2 (NFE2L2), heme oxygenase 1 (HMOX1), glutathione-disulfide reductase (GSR), and NAD(P)H quinone dehydrogenase 1 (NQO1)) in Ca9-22 cells. Moreover, WFA induces mild phosphorylation of the mitogen-activated protein kinase (MAPK) family, including extracellular signal-regulated kinases 1/2 (ERK1/2), c-Jun N-terminal kinase (JNK), and p38 expression. All WFA-induced changes were suppressed by the presence of ROS scavenger N-acetylcysteine (NAC). Therefore, these results suggest that low concentration of WFA retains potent ROS-mediated anti-migration and -invasion abilities for oral cancer cells.


2018 ◽  
Vol 119 (4) ◽  
pp. 3554-3562 ◽  
Author(s):  
Flávia Cristina P. Rosin ◽  
Marina Gabriela Teixeira ◽  
Cibele Pelissari ◽  
Luciana Corrêa

Molecules ◽  
2021 ◽  
Vol 26 (17) ◽  
pp. 5345
Author(s):  
Benjawan Wudtiwai ◽  
Anupong Makeudom ◽  
Suttichai Krisanaprakornkit ◽  
Peraphan Pothacharoen ◽  
Prachya Kongtawelert

Up-regulated expression of programmed death-ligand 1 (PD-L1) by interferon-gamma (IFN-γ) has been associated with promotion of cancer cell survival and tumor cell escape from anti-tumor immunity. Therefore, a blockade of PD-L1 expression can potentially be used as a molecular target for cancer therapy. The aim of this study was to investigate whether suppression of IFN-γ induced PD-L1 expression in two oral cancer cell lines, HN6 and HN15, by hesperidin effectively decreased cell proliferation and migration. Further, our objective was to elucidate the involvement of the signal transducer and activator of transcription 1 (STAT1) and STAT3 in the inhibition of induced PD-L1 expression by hesperidin. Our findings indicate that IFN-γ induced expression of PD-L1 protein in HN6 and HN15 via phosphorylation of STAT1 and STAT3 and that hesperidin significantly reduced that induction through suppression of phosphorylated STAT1 and STAT3 in both cell lines. Moreover, hesperidin also significantly decreased the viability, proliferation, migration, and invasion of both cell lines. In conclusion, hesperidin exerted anticancer effects against oral cancer cells through the suppression of PD-L1 expression via inactivation of the STAT1 and STAT3 signaling molecules. The findings of this study support the use of hesperidin as a potential adjunctive treatment for oral cancer.


2018 ◽  
Vol 117 (8) ◽  
pp. 738-742 ◽  
Author(s):  
Chih-Yuan Fang ◽  
Pei-Yin Chen ◽  
Dennis Chun-Yu Ho ◽  
Lo-Lin Tsai ◽  
Pei-Ling Hsieh ◽  
...  

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