Activation of NF-κB: Bridging the gap between inflammation and cancer in colitis-mediated colon carcinogenesis

Setia, Shruti; Nehru, Bimla; Sanyal, Sankar Nath

doi:10.1016/j.biopha.2013.09.003

Cited by 34 publications

(16 citation statements)

References 36 publications

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“…TNF-a, a cytokine, has been found to be involved in all the stages of carcinogenesis such as cellular transformation, promotion, survival, proliferation, angiogenesis and metastasis [2]. Our previous studies have shown that the presence of such cytokines in the inflammatory milieu might lead to the transformation of cytoplasmic inactive transcription factor, nuclear factor kB (NF-kB) to its active nuclear form, thereby leading to tumorigenesis [2]. Presently, we attempt to look further into the aspects of inflammation associated colon cancer by studying the tyrosine kinases activated MAPK/Erk pathway.…”

Section: Introductionmentioning

confidence: 99%

Upregulation of MAPK/Erk and PI3K/Akt pathways in ulcerative colitis-associated colon cancer

Setia¹,

Nehru²,

Sanyal³

2014

Biomedicine & Pharmacotherapy

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Section: Introductionmentioning

confidence: 99%

Upregulation of MAPK/Erk and PI3K/Akt pathways in ulcerative colitis-associated colon cancer

Setia¹,

Nehru²,

Sanyal³

2014

Biomedicine & Pharmacotherapy

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“…Cervical cancer is the fourth most common tumor among women in the world, with over 500,000 new cases in 2018 [1]. At present, many studies have noted that persistent inflammatory conditions play a crucial role in tumorigenesis, such as in hepatocellular carcinoma [2,3]. Chronic inflammation promotes the malignant transformation of the epithelium by stimulating free radical production and suppressing the immune system.…”

Section: Introductionmentioning

confidence: 99%

The effect of TLR4 on the growth and local inflammatory microenvironment of HPV-related cervical cancer in vivo

Jiang

Xie

Chen

et al. 2020

Infect Agents Cancer

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Background: Cervical cancer is the most common malignancy of the female lower genital tract. In our previous study, we found that TLR4 promotes cervical cancer cell growth in vitro. The aim of this study was to further explore the role of TLR4 in HPV-related cervical cancer in vivo by using a nude mouse xenograft model. Methods: Cervical cancer-derived HeLa and CaSki cells (5 × 10 7 /mL) were either stimulated with an optimal concentration of LPS for the appropriate time (HeLa cells were treated with 1 μg/mL LPS for 1 h, and CaSki cells were treated with 2 μg/mL LPS for 1.5 h) or transfected with TLR4 shRNA and then injected subcutaneously into the dorsal right posterior side of nude mice. The shortest width and longest diameter of the transplanted tumors in the nude mice were measured every 3 days.TLR4, IL-6,iNOS, IL-8,COX-2, MIP-3α, TGF-β1 and VEGF expression levels in the transplanted tumor tissue were detected by immunohistochemistry. Results: The tumor formation rate was 100% in both HeLa and CaSki nude mouse groups. The tumors grew faster, and the cachexia symptoms were more serious in the LPS groups than in the control group. In contrast, the tumors grew slower, and the cachexia symptoms were milder in the TLR4-silenced groups. TLR4, iNOS, IL-6, MIP-3α and VEGF were highly expressed in the transplanted tumor tissues from the LPS groups, and their expression levels were decreased in the TLR4-silenced groups. Conclusion: TLR4 expression is closely associated with the tumorigenesis and growth of HPV-positive cervical cancer; TLR4 promotes HPV-positive cervical tumor growth and facilitates the formation of a local immunosuppressive microenvironment. Eventually, these conditions may lead to cervical cancer development.

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“…ISO-1 downregulated the expression of MIF, NF-κB p65 and TNF-α. The NF-κB and TNF-α signaling pathways are crucial elements in inflammation and tumorigenesis, as well as cancer cell proliferation and metastasis [28][29][30][31] . Furthermore, elevated TNF-α production by many cancer cells will positively feedback in an autocrine fashion to further augment the activation of the NF-κB signaling pathway to promote cancer cell proliferation, migration and invasion 29 .…”

Section: Iso-1 Attenuated Panc-1 Single Cell Migration and Invasionmentioning

confidence: 99%

MIF inhibitor, ISO-1, attenuates human pancreatic cancer cell proliferation, migration and invasion in vitro, and suppresses xenograft tumour growth in vivo

Cheng

Wang

Song

et al. 2020

Sci Rep

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This study sought to investigate the biological effects of specific MIF inhibitor, ISO-1, on the proliferation, migration and invasion of PANC-1 human pancreatic cells in vitro, and on tumour growth in a xenograft tumour model in vivo. The effect of ISO-1 on PANC-1 cell proliferation was examined using CCK-8 cell proliferation assay. The effect of ISO-1 on collective cell migration and recolonization of PANC-1 cells was evaluated using the cell-wound closure migration assay. The effect of ISO-1 on the migration and invasion of individual PANC-1 cells in a 3-dimensional environment in response to a chemo-attractant was investigated through the use of Transwell migration/invasion assays. Quantitative real time PCR and western blot analyses were employed to investigate the effects of ISO-1 on Mif, nf-κB p65 and TNF-α mRNA and protein expression respectively. Finally, a xenograft tumor model in BALB/c nude mice were used to assess the in vivo effects of ISO-1 on PANC-1-induced tumor growth. We found high expression of MIF in pancreatic cancer tissues. We demonstrated that ISO-1 exerts anti-cancer effects on PANC-1 cell proliferation, migration and invasion in vitro, and inhibited PANC-1 cell-induced tumour growth in xenograft mice in vivo. Our data suggests that ISO-1 and its derivative may have potential therapeutic applications in pancreatic cancer.Pancreatic cancer exhibits very poor prognosis and extremely high mortality rate with a five-year survival rate of less than 5% 1-3 . As a result of its unique anatomical location, low degree of differentiation, and rapid disease development, most pancreatic malignancy presents at advances stages at the time of diagnosis 4 . Furthermore, as prominent resistance to systemic chemotherapy and radiotherapy often develops, surgical resection remains the only treatment option with curative potential 5-7 . However, less than 20% of patients are presented with this opportunity 8,9 . Despite advances in our understanding of the biology of pancreatic cancer development and progression, we are far from providing a curative answer. Therefore, there is still an urgent need for the identification and/or development of novel effective agents for the treatment of this aggressive malignancy.Macrophage migration inhibitory factor (MIF), a member of the tautomerase family of cytokines, was originally identified as a T-cell-derived factor that inhibits the random migration of macrophages 10,11 . MIF is now recognized as a pleiotropic pro-inflammatory mediator playing critical roles in the innate and adaptive immune response and the overall inflammatory cascade 12-14 . MIF expression is elevated in numerous inflammatory and autoimmune diseases correlating positively with disease severity 15,16 . Given that inflammation and immunity are intimately associated with cancer progression, severity and unfavourable prognostic outcomes, it is not surprising that MIF expression have been found to be elevated in numerous cancers including squamous carcinoma, glioblastoma, cervical adenocarcinoma, malig...

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Activation of NF-κB: Bridging the gap between inflammation and cancer in colitis-mediated colon carcinogenesis

Cited by 34 publications

References 36 publications

Upregulation of MAPK/Erk and PI3K/Akt pathways in ulcerative colitis-associated colon cancer

Upregulation of MAPK/Erk and PI3K/Akt pathways in ulcerative colitis-associated colon cancer

The effect of TLR4 on the growth and local inflammatory microenvironment of HPV-related cervical cancer in vivo

MIF inhibitor, ISO-1, attenuates human pancreatic cancer cell proliferation, migration and invasion in vitro, and suppresses xenograft tumour growth in vivo

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