NFIB promotes cell growth, aggressiveness, metastasis and EMT of gastric cancer through the Akt/Stat3 signaling pathway

Wu, Chen; Zhu, Xiaojie; Liu, Weizhen; Ruan, Tuo; Wan, Wenze; Tao, Kaixiong

doi:10.3892/or.2018.6574

Cited by 24 publications

(37 citation statements)

References 26 publications

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“…NFIB is a member of the nuclear factor family (which also includes NFIA, and NFIX). Emerging evidence has demonstrated that NFIB could not only participate in normal somatic development [22], it also acted as an oncogene and involved in tumorigenesis of several cancers, including osteosarcoma [23], glioma [24], astrocytoma [25], gastric cancer [26], breast cancer [27]. Liu et al's research showed that NFIB could suppress p21 transcription [28].…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-138-5p targets the NFIB-Snail1 axis to inhibit colorectal cancer cell migration and chemoresistance

Chen

et al. 2020

Cancer Cell Int

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Background Colorectal cancer ranks among the most lethal diseases worldwide. Although much progress has been made in research and treatment of colorectal cancer in recent years, the underlying mechanisms related to migration of the cancer cells and the reason for chemoresistance still remain unclear. In this research, we explored the underlying effect of miR-138-5p in colorectal cancer. Methods We used qRT-PCR to investigate the expression of miR-138-5p, Snail1, NFIB in colorectal cancer cells. Lentiviral vectors containing miR-138-5p mimics and inhibitors were constructed and transfected cells. Wound healing assay was applied to illustrate interferences on cell migration. Fluorouracial, doxorubicin, cisplat in were used to detect chemotherapy resistance. In order to identify target genes, bioinformatic methods were applied. Snail1 and NFIB protein expression in stable cell lines was detected using Western blot. Double luciferase and CHIP experiment were used to verify binding sites. We used rescue experiments to further explore the interactions among Snail1, NFIB and miR-138-5p. Results The expression of miR-138-5p in colorectal cancer cells was low. miR-138-5p inhibited cell migration in colorectal cancer, and could negatively regulate chemotherapy resistance. miR-138-5p targeted NFIB, and regulated Snail1 expression, which mediated colorectal cancer cell migration and chemotherapy resistance. Conclusions Our research indicates that miR-138-5p could be a crucial modulator controlling colorectal cancer cell migration and chemoresistance, by acting upon the NFIB-Snail1 axis. miR-138-5p has an emerging prospect to be exploited as a new target for colorectal cancer.

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Section: Discussionmentioning

confidence: 99%

MicroRNA-138-5p targets the NFIB-Snail1 axis to inhibit colorectal cancer cell migration and chemoresistance

Chen

et al. 2020

Cancer Cell Int

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“…After the EMT process, cells lose polarity and acquire the ability to move freely . Previous studies have reported that NFIB can induce EMT, however, the specific mechanism is still unclear . In our study, we explored the link between NFIB and EMT‐TFs and discovered that NFIB could promote snail expression by binding to the Snail promoter.…”

Section: Discussionmentioning

confidence: 89%

“…NFIB was reported to bind to the EZH2 promoter and promote EZH2 expression, which could activate the PI3K/AKT pathway . Wu et al discovered that NFIB can activate the Akt/Stat3 signaling pathway in gastric cancer. However, the relationship between the effects of NFIB on the biological behavior of CRC and the activation of the Akt pathway has not been reported.…”

Section: Discussionmentioning

confidence: 99%

“…18 Previous studies have reported that NFIB can induce EMT, however, the specific mechanism is still unclear. 11 In our study, we explored the link between NFIB and EMT-TFs and discovered that NFIB could promote snail expression by binding to the Snail promoter. Snail is a zinc finger protein that can mediate EMT through downregulation of cell adhesion molecules, such as E-cadherin, by binding several Eboxes located in the promotor region.…”

Section: Discussionmentioning

confidence: 99%

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Nuclear factor I/B promotes colorectal cancer cell proliferation, epithelial‐mesenchymal transition and 5‐fluorouracil resistance

et al. 2018

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Nuclear factor I/B (NFIB) is a widely studied transcription factor that participates in tumor progression; nevertheless, studies on NFIB in colorectal cancer (CRC) are limited. In our study, Western blot and RT‐PCR analyses showed that NFIB was overexpressed in CRC tissues and cell lines, which was consistent with our bioinformatic analysis results. Furthermore, NFIB expression was closely related to the TNM stage of CRC. NFIB promoted cell proliferation and migration and inhibited cell apoptosis in vitro. Meanwhile, we discovered that NFIB accelerated xenograft tumor growth in vivo. In addition, NFIB weakened the sensitivity of CRC cells to 5‐fluorouracil (5‐FU). NFIB induced epithelial‐mesenchymal transition (EMT) by upregulating snail expression, which was accompanied by decreased E‐cadherin and Zo‐1 expression and increasedd Vimentin expression. Because the Akt pathway plays an important role in CRC progression, we examined whether there was a correlation between NFIB and the Akt pathway in cell proliferation and migration. Our results showed that NFIB promoted cell proliferation and increased 5‐FU resistance by activating the Akt pathway. In summary, our findings suggested that NFIB induced EMT of CRC cells via upregulating snail expression and promoted cell proliferation and 5‐FU resistance by activating the Akt pathway.

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“…Interestingly, western blot analyses revealed that CRP significantly elevated extracellular signal-regulated kinases (ERKs) levels and IL-6 notably elevated signal transducer and activator of transcription 3 (STAT3) levels [36]. Therefore, researchers stated that CRP activates MAPK/ERK pathway and IL-6 activates Akt/STAT3 pathway were both strongly associated with carcinogenesis [37][38][39][40]. ERKs have a pleiotropic effect on neoplasms where they activate pro-survival pathways leading to cell proliferation and migration, modulate apoptosis, cell differentiation and senescence and according to research by Salaroglio et al ERKs this plays a major role in tumor resistance for immune system responses and chemotherapy [37].…”

Section: Increased Crp As a Bad Prognostic Sign -Potential Mechanismmentioning

confidence: 99%

C-reactive Protein as a Diagnostic and Prognostic Factor of Endometrial Cancer

Socha¹,

Malinowski²,

Wartęga³

et al. 2020

Preprint

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Endometrial Cancer (EC) is the sixth most commonly occurring cancer in women with 380 000 cases in 2018. Sadly, EC morbidity and mortality are continuously increasing, therefore the medical society have a substantial need for an accurate and inexpensive diagnostic test for EC early detection and a prognostic tool for treatment planning and evaluation. Considering experience with different types of cancers C-reactive protein (CRP) appears to be a promising diagnostic and prognostic factor. Aiming to investigate its potential and in view of EC authors, this paper reviewed the following databases for metanalysis, randomized controlled trials and review articles published up to June 2020: Pubmed, Scopus, Google scholar and ClinicalKey. Studies indicate CRP >3.33 mg/l correlate with EC incidence with HR = 2.29 (p<0.05). Moreover, High-sensitivity CRP assay allows to detect CRP in very low concentrations and distinguish patients with endometriosis, soft tissue sarcomas and possibly EC. Preoperational and postoperational CRP, as well as its dynamic change are independent prognostic factors for EC and are more reliable if analyzed together. However, CRP-to-albumin ratio as well as Glasgow Prognostic Scale have greater prognostic value that CRP alone. Additionally, CRP is possibly a mediator of carcinogenesis and cancer progression through activation of inter alia FcgRs/MAPK/ERK, FcgRs/IL-6/AKT/STAT3 and FcgRs/NF-κB/NLRP3 pathways.

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NFIB promotes cell growth, aggressiveness, metastasis and EMT of gastric cancer through the Akt/Stat3 signaling pathway

Cited by 24 publications

References 26 publications

MicroRNA-138-5p targets the NFIB-Snail1 axis to inhibit colorectal cancer cell migration and chemoresistance

MicroRNA-138-5p targets the NFIB-Snail1 axis to inhibit colorectal cancer cell migration and chemoresistance

Nuclear factor I/B promotes colorectal cancer cell proliferation, epithelial‐mesenchymal transition and 5‐fluorouracil resistance

C-reactive Protein as a Diagnostic and Prognostic Factor of Endometrial Cancer

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