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

View Article: PubMed Central - PubMed

ABSTRACT

Background: Recent 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/methods: The 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).

Results: We 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.

Conclusions: Our results suggest that TNF-α enhances the invasion and metastasis ability of OSCC cells via the NF-κB signaling pathway.

No MeSH data available.


OSCC cells were treated with TNF-α (10 ng/ml) for the indicated times. (A) The mRNA level of IKKβ and p65 was analyzed by real-time RT-PCR. β-actin was used as a control. (B) Western blot analysis was performed to assess the expression of IKKβ and p65 at the protein level. β-actin was used as a loading control. (C) Statistical analysis of western blot analysis. Each bar represents the mean ±S.D. * P<0.05, ** P<0.05, *** P<0.05, **** P<0.05.
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f1-medscimonitbasicres-23-141: OSCC cells were treated with TNF-α (10 ng/ml) for the indicated times. (A) The mRNA level of IKKβ and p65 was analyzed by real-time RT-PCR. β-actin was used as a control. (B) Western blot analysis was performed to assess the expression of IKKβ and p65 at the protein level. β-actin was used as a loading control. (C) Statistical analysis of western blot analysis. Each bar represents the mean ±S.D. * P<0.05, ** P<0.05, *** P<0.05, **** P<0.05.

Mentions: We observed that IKKβ and p65 in HN4, HN6, and CAL27 cells increased significantly after TNF-α stimulation. After being treating with 10 ng/ml TNF-α for 0 h, 3 h, 6 h, 12 h, 24 h, 48 h, and 72 h, RT-PCR and western blot analysis revealed that the level of IKKβ and p65 were significantly increased after 24 h, 48 h, and 72 h (Figure 1A, 1B). Western blot analysis showed statistically significant differences (Figure 1C). The above results indicate that TNF-α activates the NF-κB pathway in oral cancer cells.


TNF-Alpha Promotes Invasion and Metastasis via NF-Kappa B Pathway in Oral Squamous Cell Carcinoma
OSCC cells were treated with TNF-α (10 ng/ml) for the indicated times. (A) The mRNA level of IKKβ and p65 was analyzed by real-time RT-PCR. β-actin was used as a control. (B) Western blot analysis was performed to assess the expression of IKKβ and p65 at the protein level. β-actin was used as a loading control. (C) Statistical analysis of western blot analysis. Each bar represents the mean ±S.D. * P<0.05, ** P<0.05, *** P<0.05, **** P<0.05.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC5391804&req=5

f1-medscimonitbasicres-23-141: OSCC cells were treated with TNF-α (10 ng/ml) for the indicated times. (A) The mRNA level of IKKβ and p65 was analyzed by real-time RT-PCR. β-actin was used as a control. (B) Western blot analysis was performed to assess the expression of IKKβ and p65 at the protein level. β-actin was used as a loading control. (C) Statistical analysis of western blot analysis. Each bar represents the mean ±S.D. * P<0.05, ** P<0.05, *** P<0.05, **** P<0.05.
Mentions: We observed that IKKβ and p65 in HN4, HN6, and CAL27 cells increased significantly after TNF-α stimulation. After being treating with 10 ng/ml TNF-α for 0 h, 3 h, 6 h, 12 h, 24 h, 48 h, and 72 h, RT-PCR and western blot analysis revealed that the level of IKKβ and p65 were significantly increased after 24 h, 48 h, and 72 h (Figure 1A, 1B). Western blot analysis showed statistically significant differences (Figure 1C). The above results indicate that TNF-α activates the NF-κB pathway in oral cancer cells.

View Article: PubMed Central - PubMed

ABSTRACT

Background: Recent evidence reveals that the inflammatory microenvironment is associated with tumor migration, invasion, and metastasis. Tumor necrosis factor-&alpha; (TNF-&alpha;) play a vital role in regulation of the inflammatory process in tumor development. Nuclear factor-kappa B (NF-&kappa;B) 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-&kappa;B on the invasion and migration of oral squamous cell carcinoma (OSCC).

Material/methods: The IKK&beta; 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-&alpha; and BAY11-7082 on the migration of the OSCC cell lines (HN4, HN6, and CAL27).

Results: We observed a significant increase of the expression level of IKK&beta; and p65 in OSCC cells from the experimental group at 24 h, 48 h, and 72 h after TNF-&alpha; stimulation. Invasion and metastasis of OSCC cells was obviously improved after the TNF-&alpha; stimulation. Invasion and metastasis ability of OSCC cells was inhibited in the suppression group, and no significant changes were observed in expression level of IKK&beta; and p65 after the use of BAY11-7082.

Conclusions: Our results suggest that TNF-&alpha; enhances the invasion and metastasis ability of OSCC cells via the NF-&kappa;B signaling pathway.

No MeSH data available.