STC1 and NF-κB p65 (Rel A) is Constitutively Activated in Colorectal Cancer

Rezapour, Saleheh; Bahrami, Tayyeb; Hashemzadeh, Shahryar; Estiar, Mehrdad Asghari; Nemati, Masoumeh; Ravanbakhsh, Reyhaneh; Feizi, Mohammad Ali Hosseinpour; Kafil, Hossein Samadi; Pouladi, Nasser; Ghojazadeh, Morteza; Sakhinia, Ebrahim

doi:10.7754/clin.lab.2015.150827

Cited by 21 publications

(17 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Some studies have suggested the anti-apoptosis effect of STC1, such as colorectal cancer [27, 28], breast cancer [19, 29], glioma tumor [11, 30], thyroid cancer [20, 31], ovarian cancer [32, 33] and so on. Others indicated the pro-apoptosis effects.…”

Section: Discussionmentioning

confidence: 99%

STC1 promotes cell apoptosis via NF-κB phospho-P65 Ser536 in cervical cancer cells

Jiang

Liu

et al. 2017

Oncotarget

View full text Add to dashboard Cite

Stanniocalin-1 (STC1) is a secreted glycoprotein hormone and involved in various types of human malignancies. Our previous studies revealed that STC1 inhibited cell proliferation and invasion of cervical cancer cells through NF-κB P65 activation, but the mechanism is poorly understood. In our studies, we found overexpression of STC1 promoted cell apoptosis while silencing of STC1 promoted cell growth of cervical cancer. Phospho-protein profiling and Western blotting results showed the expression of NF-κB related phosphorylation sites including NF-κB P65 (Ser536), IκBα, IKKβ, PI3K, and AKT was altered in STC1-overexpressed cervical cancer cells. Moreover, PI3K inhibitor LY294002, AKT-shRNA and IκBα-shRNA could decrease the protein content of phospho-P65 (Ser536), phospho-IκBα, phospho-AKT and phospho-IKKβ while increasing the level of P65 compared to STC1 overexpression groups in cervical cancer cells. Also, PI3K inhibitor LY294002, AKT-shRNA and IκBα-shRNA elevated the percentage of apoptosis and suppressed the G1/S transition in those cells. Additionally, STC1 level was decreased in cervical cancer, especial in stage II and III. The results of immunohistochemistry for the cervical cancer microarray showed that a lower level of STC1, phospho-PI3K and P65 protein expression in tumor tissues than that in normal tissues, and a higher level of phospho-P65 protein expression in tumor tissues, which is consistent with the results of the Western blotting. These data demonstrated that STC1 can promote cell apoptosis via NF-κB phospho-P65 (Ser536) by PI3K/AKT, IκBα and IKK signaling in cervical cancer cells. Our results offer the first mechanism that explains the link between STC1 and cell apoptosis in cervical cancer.

show abstract

Section: Discussionmentioning

confidence: 99%

STC1 promotes cell apoptosis via NF-κB phospho-P65 Ser536 in cervical cancer cells

Jiang

Liu

et al. 2017

Oncotarget

View full text Add to dashboard Cite

show abstract

“…INHBA has a significant relationship with the occurrence and development of gastric, esophageal, and ovarian cancers, and studies have reported that the immunosuppressive treatment of INHBA can reduce the rate of deterioration of gastric and ovarian cancers [17][18][19]. STC1OXTR, and UCN can promote the metastasis of colon cancer [20][21][22][23].…”

Section: Discussionmentioning

confidence: 99%

Prediction and identification of immune genes related to the prognosis of patients with colon adenocarcinoma and its mechanisms

Chen

et al. 2020

Preprint

View full text Add to dashboard Cite

Abstract Background Colon adenocarcinoma(COAD) is a type of gastrointestinal tumor with a high degree of malignancy, and its immunotherapy method has been stagnant. Recently, with the development of network databases and the development of bioinformatics tools, we can analyze the data in the current database to find out which genes may be the target of immunotherapy for COAD. Methods We use various codes and packages in R language to analyze the downloaded data, construct a riskScore model of immune genes and clinical data, and use Cox regression analysis to explore the clinical relationship between riskScore and COAD. Results We found that seven immune genes associated with the survival prognosis of COAD were related to the construction of a riskScore model. And Cox regression analysis found that there was clinical significance and statistical significance between the riskScore model and clinical data of COAD. Some traditional immune microenvironment cells also increase their cell content with the increase of riskScore. Conclusions We found 7 immune genes (SLC10A2, CXCL3, IGHV5-51, INHBA, STC1, UCN, and OXTR) that affect the clinical prognosis of COAD patients and can construct a riskScore model. It may be a target for future COAD immunotherapy.

show abstract

“…Dong Yang et al identified that P65 induced miR-17 transcription by binding its promoter elements to regulate proliferation of vascular smooth muscle cells under inflammation [45]. Rezapour S et al reported that P65 was constitutively activated in colorectal cancer [35]. Other reports proved that P65 might serve as an activating transcription factor in several types of human cancers [19; 23].…”

Section: Discussionmentioning

confidence: 99%

Preclinical Study: Sunitinib-suppressed MiR-452-5p Facilitates Renal Cancer Cell Invasion and Metastasis Through Modulating SMAD4/SMAD7/EMT Signals

Zhai

Zhang

et al. 2018

Preprint

View full text Add to dashboard Cite

Although microRNAs (miRNAs) have been revealed as crucial modulators in tumor metastasis and target therapy, our understanding of their roles in metastatic renal cell carcinoma (mRCC) and Sunitinib treatment is limited. Here, We focused on 2 published microarray data to select out our anchored miRNA which was downregulated after Sunitinib treatment while upregulated in metastasis RCC tissues.Then we discovered that treating with Sunitinib, the targeted receptor tyrosine kinase inhibitor (TKI), inhibited renal cell migration and invasion via attenuating the expression of miR-452-5p. The novel identified miR-452-5p was upregulated and associated with poor prognosis in RCC. Preclinical studies using multiple RCC cells and xenografts model illustrated that miR-452-5p could promote RCC cell migration and invasion in vitro and in vivo. Mechanistically, P65 could directly bind to the miR-452-5p promoter and thus transcriptionally induce miR-452-5p expression, which led to post-transcriptionally abrogate SMAD4 expression, thus inhibition of its downstream signals including SMAD7 and EMT (Epithelial-Mesenchymal Transition) associated genes. Our study presented a road map for targeting this newly identified miR-452-5p and its SMAD4/SMAD7/EMT signals pathway, which imparted a new potential therapeutic strategy for mRCC treatment.

show abstract

STC1 and NF-κB p65 (Rel A) is Constitutively Activated in Colorectal Cancer

Cited by 21 publications

References 0 publications

STC1 promotes cell apoptosis via NF-κB phospho-P65 Ser536 in cervical cancer cells

STC1 promotes cell apoptosis via NF-κB phospho-P65 Ser536 in cervical cancer cells

Prediction and identification of immune genes related to the prognosis of patients with colon adenocarcinoma and its mechanisms

Preclinical Study: Sunitinib-suppressed MiR-452-5p Facilitates Renal Cancer Cell Invasion and Metastasis Through Modulating SMAD4/SMAD7/EMT Signals

Contact Info

Product

Resources

About