scholarly journals Synthetic curcumin analog: inhibiting the invasion, angiogenesis, and metastasis in human laryngeal carcinoma cells via NF-kB pathway

Author(s):  
Kumaravel Mohankumar ◽  
Arul Prakash Francis ◽  
Sankar Pajaniradje ◽  
Rukkumani Rajagopalan
2021 ◽  
Author(s):  
Kumaravel Mohankumar ◽  
Arul Prakash Francis ◽  
Sankar Pajaniradje ◽  
Rukkumani Rajagopalan

Abstract Laryngeal carcinoma, the most common among head and neck squamous cell carcinoma (HNSCC) induces 1% of all cancer deaths. Curcumin, the active constituent of turmeric is more effective in the treatment of various cancer. In the present study, with an aim to explore the mechanistic role of BDMC-A as a chemotherapeutic agent, we have investigated the inhibitory effect of BDMC-A on invasion, angiogenesis, and metastasis in Hep-2 cells and compared it with curcumin. Curcumin and BDMC-A treated Hep-2 cells were quantified using western blotting and RT-PCR technique to investigate the effect of Curcumin and BDMC-A on transcription factors involved in signal transduction cascade, invasion and angiogenesis associated markers. Pro-inflammatory markers of curcumin and BDMC-A treated Hep-2 cells were estimated using the ELISA kit. The results showed that BDMC-A might exhibit the anti-cancer activity by inhibiting transcription factors mainly NF-κB, p65, c-Jun, c-Fos, STAT3, 5, PPAR-γ and β-catenin, which are responsible for tumor progression and malignancy. Downregulation of MMP-9, VEGF, IL-6 and IL-8 and upregulation of TIMP-2 levels further supports the anti-tumor potential of BDMC-A. Our overall results revealed that BDMC-A more effectively inhibited the markers of invasion, angiogenesis and metastasis in comparison with curcumin.


2011 ◽  
Vol 62 (2) ◽  
pp. 139-146 ◽  
Author(s):  
Ksenija Durgo ◽  
Sandra Kostić ◽  
Katarina Gradiški ◽  
Draženka Komes ◽  
Maja Osmak ◽  
...  

Genotoxic Effects of Green Tea Extract on Human Laryngeal Carcinoma Cells In VitroGreen tea (Camellia sinensis) contains several bioactive compounds which protect the cell and prevent tumour development. Phytochemicals in green tea extract (mostly flavonoids) scavenge free radicals, but also induce pro-oxidative reactions in the cell. In this study, we evaluated the potential cytotoxic and prooxidative effects of green tea extract and its two main flavonoid constituents epigallocatechin gallate (EGCG) and epicatechin gallate (ECG) on human laryngeal carcinoma cell line (HEp2) and its cross-resistant cell line CK2. The aim was to see if the extract and its two flavonoids could increase the sensitivity of the cisplatin-resistant cell line CK2 in comparison to the parental cell line. The results show that EGCG and green tea extract increased the DNA damage in the CK2 cell line during short exposure. The cytotoxicity of EGCG and ECG increased with the time of incubation. Green tea extract induced lipid peroxidation in the CK2 cell line. The pro-oxidant effect of green tea was determined at concentrations higher than those found in traditionally prepared green tea infusions.


ORL ◽  
2008 ◽  
Vol 70 (3) ◽  
pp. 168-175 ◽  
Author(s):  
Xiu-mei Chen ◽  
Xin-yong Luan ◽  
Da-peng Lei ◽  
Xiao-jie Ma ◽  
Xue-xia Liu ◽  
...  

2019 ◽  
Vol 2019 ◽  
pp. 1-6
Author(s):  
Dan Xu ◽  
Da Wei Li ◽  
Jin Xie ◽  
Xin Wei Chen

This study aimed at clarifying the mechanism and role of survivin in hypoxia-induced multidrug resistance (MDR) of laryngeal carcinoma cells. Human laryngeal cancer cells were incubated under hypoxia or normoxia. The expression of survivin was silenced by performing RNA interference. Additionally, by Western blot and real-time quantitative RT-PCR, survivin expression was detected. The sensitivity of human laryngeal carcinoma cells to multiple drugs was measured by CCK-8 assay. Meanwhile, the apoptosis of cells induced by cisplatin or paclitaxel was assessed by Annexin-V/propidium iodide staining analysis. Under hypoxic conditions, the upregulation of survivin was abolished by RNA interference. Then, CCK-8 analysis demonstrated that the sensitivity to multiple agents of laryngeal carcinoma cells could be increased by inhibiting survivin expression (P<0.05). Moreover, Annexin-V/propidium iodide staining analysis revealed that decreased expression of survivin could evidently increase the apoptosis rate of laryngeal carcinoma cells that were induced by cisplatin or paclitaxel evidently (P<0.05). Our data suggests that hypoxia-elicited survivin may exert a pivotal role in regulating hypoxia-induced MDR of laryngeal cancer cells by preventing the apoptosis of cells induced by chemotherapeutic drug. Thus, blocking survivin expression in human laryngeal carcinoma cells may provide an avenue for gene therapy.


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