CREB1

Official Full Name

cAMP responsive element binding protein 1

Organism

Homo sapiens

GeneID

1385

Background

This gene encodes a transcription factor that is a member of the leucine zipper family of DNA binding proteins. This protein binds as a homodimer to the cAMP-responsive element, an octameric palindrome. The protein is phosphorylated by several protein kinases, and induces transcription of genes in response to hormonal stimulation of the cAMP pathway. Alternate splicing of this gene results in several transcript variants encoding different isoforms. [provided by RefSeq, Mar 2016]

Synonyms

CREB; CREB-1;

Cat.No.	Product Name	Price

Cat.No.	Product Name	Price

Cat.No.	Product Name	Price

Cat.No.	Product Name	Price

Detailed Information

Recent Research Progress

cAMP response element binding protein 1 (CREB1) is a well characterized transcription factor belonging to the basic ieucine zipper (bZIP) family. As a transcriptional activator, CREB1 binds to a conserved cAMP-response element (CRE) on the promoter and mediates transcriptional responses to various stimuli, including neurotransmitters, hormones, membrane depolarization, and growth and neurotrophic factors, thereby acting as a mediator between different signal pathways and the downstream target genes transcription. Interestingly, there is increasing evidence that CREB1 has potential carcinogenic functions and plays a key role in carcinogenesis and cancer progression.

CREB1 and CRC

CREB1 acts as a transcription factor for the ribonucleotide reductase M2 (RRM2) gene in human colorectal cancer (CRC). CREB1 directly binds to the promoter of the RRM2 gene and induces its transcriptional activation. Knockdown of CREB1 reduced the expression of RRM2 at mRNA and protein levels. Furthermore, knockdown of RRM2 attenuated CREB1-induced aggressive phenotypes of CRC cells in vitro and in vivo. A decrease in disease survival rate was observed in CRC patients with high expression levels of CREB1 or RRM2. The results indicate that CREB1 is a key transcription factor of RRM2, which promotes tumor aggressiveness and suggests a significant correlation between CREB1 and RRM2 in CRC specimens. These may offer the possibility that CREB1 and RRM2 can be used as biomarkers or targets for CRC diagnosis and treatment.

CREB1 and GC

Gastric cancer (GC) is the fourth most common cancer in the world and the second leading cause of cancer-related mortality in humans. The expression of miR-122 was significantly reduced in GC tissues and cell lines, and the decrease in expression was significantly associated with the invasive clinic pathological features of the patient. Moreover, overexpression of miR-122 significantly inhibited proliferation, migration and invasion in GC cell lines. Furthermore, CREB1 was identified as a direct target of miR122 and its expression was inversely correlated with miR-122 expression in GC tissues. Overexpression of CREB1 rescued the inhibitory effect of miR-122 on proliferation, migration and invasion of GC cells. Furthermore, miR-122 has been demonstrated miR-122 inhibited GC tumor genesis in vivo by repressing CREB1 expression. These findings suggest that miR-122 may function as a tumor suppressor in GC and could serve as a promising candidate for therapeutic applications regarding GC treatment.

CREB1 and glioma

Glioma originates from glial cells in the brain, accounting for about 45% of all intracranial tumors. The characteristic of glioma is invasive growth, as well as there is no obvious boundary between normal brain tissue and glioma tissue, so it is difficult to resect completely with worst prognosis. The metabolism of glioma follows the Warburg effect. Previous studies have shown that GLUT1, as a carrier of glucose transporters, affected the Warburg effect. Related studies have demonstrated that CREB1 protein regulates the expression of GLUT1, thus mediating glucose transport in cells. Recent experiments have revealed that the CREB1 can affect the glucose transport of glioma cells by regulating the expression of GLUT1, which control the metabolism of glioma and affects the progression of glioma.

In addition, related studies have shown that CREB1 is associated with a variety of diseases, such as major depression (MDD), diabetes. In conclusion, CREB1 plays an important role in a variety of diseases and mechanisms of cancer development. Therefore, further study of the function of CREB1 will provide new insights into the mechanisms of various diseases and have great potential for future clinical treatment.

References:

Qian Jin, et al. MiR-1224-5p acts as a tumor suppressor by targeting CREB1 in malignant gliomas. Mol Cell Biochem, 2015, 403:33–41
Li Qinqin, et al. CREB1-driven expression of miR-320a promotes mitophagy by down-regulating VDAC1 expression during serum starvation in cervical cancer cells. Oncotarget, 2015, 6:33
Fang Zejun, et al. CREB1 directly activates the transcription of ribonucleotide reductase small subunit M2 and promotes the aggressiveness of human colorectal cancer. Oncotarget, 2016, 7: 47
Wang YaWen, et al. High expression of cAMP responsive element binding protein 1 (CREB1) is associated with metastasis, tumor stage and poor outcome in gastric cancer. Oncotarget, 2015, 6: 12
Rao Min, et al. Knockdown of CREB1 inhibits tumor growth of human gastric cancer in vitro and in vivo. Oncology Reports, 2017, 37: 3361-3368
Naomi E, et al. Essential role for cyclic-AMP responsive element binding protein 1 (CREB) in the survival of acute lymphoblastic leukemia. Oncotarget, 2015, 6: 17

Quick Inquiry

Interested in learning more?

Contact us today for a free consultation with the scientific team and discover how Creative Biogene can be a valuable resource and partner for your organization.

Request a quote today!

Inquiry