The importance of oncogenic transcription factors for oral cancer pathogenesis and treatment

Yedida, Govinda; Nagini, Siddavaram; Mishra, Rajakishore

doi:10.1016/j.oooo.2013.02.010

Cited by 18 publications

(7 citation statements)

References 131 publications

(116 reference statements)

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“…Cancer cells are more dependent on transcription factors than are normal cells. The growth of cancer cells is inhibited and the apoptosis of cancer cells is promoted through targeted inhibition of transcription factors and signaling pathways [21]. TNF-α promotes oral cancer cell invasion and metastasis, which relies on NF-κB signaling pathway activation [22,23].…”

Section: Discussionmentioning

confidence: 99%

TNF-Alpha Promotes Invasion and Metastasis via NF-Kappa B Pathway in Oral Squamous Cell Carcinoma

Tang

Tao

Fang

et al. 2017

Med Sci Monit Basic Res

116

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BackgroundRecent evidence reveals that the inflammatory microenvironment is associated with tumor migration, invasion, and metastasis. Tumor necrosis factor-α (TNF-α) play a vital role in regulation of the inflammatory process in tumor development. Nuclear factor-kappa B (NF-κB) is one of the key transcription factors which regulate processes in tumor promotion. The aim of this study was to explore the role of NF-κB on the invasion and migration of oral squamous cell carcinoma (OSCC).Material/MethodsThe IKKβ and p65 mRNA and protein levels were determined by quantitative RT-PCR and western blot. Wound scratch healing assays and transwell migration assays were used to evaluate the effect of TNF-α and BAY11-7082 on the migration of the OSCC cell lines (HN4, HN6, and CAL27).ResultsWe observed a significant increase of the expression level of IKKβ and p65 in OSCC cells from the experimental group at 24 h, 48 h, and 72 h after TNF-α stimulation. Invasion and metastasis of OSCC cells was obviously improved after the TNF-α stimulation. Invasion and metastasis ability of OSCC cells was inhibited in the suppression group, and no significant changes were observed in expression level of IKKβ and p65 after the use of BAY11-7082.ConclusionsOur results suggest that TNF-α enhances the invasion and metastasis ability of OSCC cells via the NF-κB signaling pathway.

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Section: Discussionmentioning

confidence: 99%

TNF-Alpha Promotes Invasion and Metastasis via NF-Kappa B Pathway in Oral Squamous Cell Carcinoma

Tang

Tao

Fang

et al. 2017

Med Sci Monit Basic Res

116

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“…These cells contribute to tumor initiation, promote resistance to chemoradiation treatment, support invasion/metastasis, and cause cancer recurrence. A number of oncogenic transcription factors (OTFs) are activated and participated in oral cancer disease progression 10 . The embryonic stem cell‐specific transcription factor (TF) Nanog is expressed in various cancers including OSCC 11 …”

Section: Introductionmentioning

confidence: 99%

Pluripotency transcription factor Nanog and its association with overall oral squamous cell carcinoma progression, cisplatin‐resistance, invasion and stemness acquisition

et al. 2020

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Background: Cisplatin-resistant oral squamous cell carcinoma (OSCC) cells acquire stem-like characteristics and are difficult to treat. Nanog is a transcription factor and needed for maintenance of pluripotency, but its transcription-promoting role in OSCC progression and cisplatin resistance is poorly understood. Methods: Here, 110 fresh human tissue specimens of various stages, including invasive (N 1-3)/chemoradiation-resistant OSCC samples, cisplatin-resistant (CisR-SCC-4/-9) OSCC cells/parental cells, photochemical ECGC, and siRNA (Nanog) were used. Results: Nanog overexpression was associated with overall progression, chemoresistance, and invasion of OSCC. Nanog recruitment to c-Myc, Slug, Ecadherin, and Oct-4 gene promoter was observed. Positive correlation of Nanog protein expression with c-Myc, Slug, cyclin D1, MMP-2/-9, and Oct-4 and negative correlation with E-cadherin gene expression were found. Knockdown of Nanog and treatment of epicatechin-3-gallate reversed cisplatin resistance and diminished invasion/migration potential. Conclusion: Nanog directly participated in the regulation of Slug, E-cadherin, Oct-4, and c-Myc genes, causing cisplatin resistance/recurrence of OSCC.

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“…4 Continuous activation of cancer-causing signaling pathways has consistently shown a connection with the development of fundamental cancer traits, including increased cell proliferation, evasion of programmed cell death, invasion, and the stimulation of blood vessel formation (angiogenesis). 5,6 Speci cally, the PI3K/Akt and NF-κB signaling pathways exhibit the most signi cant degree of dysfunction across diverse malignant tumors. 7,8 Phosphatidylinositol-3-kinase (PI3K) is an initial lipid kinase that becomes active due to the in uence of different growth factors through receptor tyrosine kinases.…”

Section: Introductionmentioning

confidence: 99%

Modulatory effect of α-Bisabolol on induced apoptosis via mitochondrial and NF-κB/Akt/PI3K Signaling pathways in MCF-7 breast cancer cells

Arjunan,

Balaraman,

Alquraishi

2024

Preprint

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Breast cancer is a highly feared form of cancer that predominantly affects women. In pursuing effective treatments, herbal medicine has garnered attention as a viable resource. It holds promise as an alternative approach for managing and combating breast cancer. The primary objective of the research was to explore how α-Bisabolol hinders the growth of MCF-7 human breast cancer cells and decipher its molecular mechanisms of reducing cell proliferation and promoting apoptosis. In the experiment, cultured MCF-7 cells were divided into four distinct groups: The first group functioned as the control, whereas the second, third, and fourth groups received separate treatments of α-Bisabolol at varying concentrations. After allowing the cells to incubate for a 24-hour, we examined them to assess any alterations in their morphology after applying α-Bisabolol. This treatment led to the suppression of cell growth, an elevation in the generation of reactive oxygen species (ROS) and the initiation of apoptosis. Furthermore, examination through western blot and real-time PCR unveiled that cell treated with α-Bisabolol exhibited reduced levels of the cell survival gene Bcl-2, alongside elevated levels of the pro-apoptotic genes Bax, Bad, Caspase-3, Caspase-9, and cytochrome c. Meanwhile, NF-κB, p-PI3K, and p-Akt proteins were downregulated in α-Bisabolol treated cells. These results suggest that α-Bisabolol diminishes the cell viability of MCF-7 cells and triggers cellular apoptosis through both the mitochondrial pathway and the NF-κB/Akt/PI3K signaling pathways.

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The importance of oncogenic transcription factors for oral cancer pathogenesis and treatment

Cited by 18 publications

References 131 publications

TNF-Alpha Promotes Invasion and Metastasis via NF-Kappa B Pathway in Oral Squamous Cell Carcinoma

TNF-Alpha Promotes Invasion and Metastasis via NF-Kappa B Pathway in Oral Squamous Cell Carcinoma

Pluripotency transcription factor Nanog and its association with overall oral squamous cell carcinoma progression, cisplatin‐resistance, invasion and stemness acquisition

Modulatory effect of α-Bisabolol on induced apoptosis via mitochondrial and NF-κB/Akt/PI3K Signaling pathways in MCF-7 breast cancer cells

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