Downregulation of MiR-1297 predicts poor prognosis and enhances gastric cancer cell growth by targeting CREB1

Gao, Wencang; Cao, Ying; Guo, Piaoting; Bao, Xiaoyan; Zhu, Hongye; Zheng, Jian; Cheng, Yong; Chen, Dong; Yu, Shenquan; Chen, Bin-Hai; Zhou, Shaoling; DeXiang, Pang; Chen, Weijian

doi:10.1016/j.biopha.2018.05.094

Cited by 27 publications

(19 citation statements)

References 16 publications

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“…17 As for in GC, an inhibitor of CREB1, miR-1297, was found to be poorly existed in GC patients and positively correlated with survival of patients. 18 Promotion of CREB1 in cancer has also been evidenced in several tumor cell types involving bladder cancer, 19 colorectal cancer 20 and glioma 21 cells. Likewise, high-expression profiles of CREB1 have also been found in GC cell lines and its downregulation led to declines in growth and migration of SGC-7901 cells.…”

Section: Discussionmentioning

confidence: 99%

<p>CREB1 Suppresses Transcription of microRNA-186 to Promote Growth, Invasion and Epithelial–Mesenchymal Transition of Gastric Cancer Cells Through the KRT8/HIF-1α Axis</p>

Huang

Liu

Jiang

et al. 2020

CMAR

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Background: The cAMP response element-binding protein 1 (CREB1) was initiated as a potential target for cancer treatment. This research was conducted to probe the effect of CREB1 in the progression of gastric cancer (GC) and the molecules involved. Materials and Methods: CREB1 expression in GC tissues and cell lines (AGS and MKN-45) as well as that in normal tissues and in gastric mucosa cell line (GES-1) was detected. The correlation between CREB1 expression and prognosis of GC patients was determined. Artificial silencing of CREB1 was introduced to evaluate its effect on biological behaviors of GC cells. The target microRNA (miRNA) of CREB1 and the target mRNA of miR-186 were predicted and validated. Altered expression of miR-186, KRT8 and HIF-1α was introduced to confirm their functions in GC progression. Results: CREB1 was abundantly expressed in GC tissues and cells and linked to dismal prognosis in patients. Silencing of CREB1 or upregulation of miR-186 suppressed the malignant behaviors such as growth, epithelial-mesenchymal transition (EMT) and invasion of GC cells, while artificial overexpression of KRT8 led to reversed trends. KRT8 was a target mRNA of miR-186, and CREB1 transcriptionally suppressed miR-186 expression to further up-regulate KRT8. KRT8 was also found to increase HIF-1α expression. Upregulation of HIF-1α was found to block the suppressing role of CREB1 silencing in GC cell malignancy. Conclusion: This study evidenced that silencing of CREB1 inhibits growth, invasion, EMT and resistance to apoptosis of GC cells involving the upregulation of miR-186 and the following downregulation of KRT8 and HIF-1α.

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Section: Discussionmentioning

confidence: 99%

<p>CREB1 Suppresses Transcription of microRNA-186 to Promote Growth, Invasion and Epithelial–Mesenchymal Transition of Gastric Cancer Cells Through the KRT8/HIF-1α Axis</p>

Huang

Liu

Jiang

et al. 2020

CMAR

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“…In fact, a prior study showed miR‐1284 might modulate multidrug resistance of GC cells by targeting specific genes . The miR‐1297 expression found to be remarkably lower in GC tissue and suppress GC cell growth by inhibiting the expression of CREB1 …”

Section: Resultsmentioning

confidence: 98%

Function and regulation annotation of up‐regulated long non‐coding RNA LINC01234 in gastric cancer

Zhu

Luo

Korakkandan

et al. 2020

Clinical Laboratory Analysis

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Background Accumulated evidences indicate that long non‐coding RNAs (lncRNAs) participate in many biological mechanisms. Moreover, it acts as an essential regulator in various human diseases such as gastric cancer (GC). Nevertheless, the comprehensive regulatory roles and clinical significance of most lncRNAs in GC are not fully understood. Methods In this research, our aim was to investigate the underlying mechanism of lncRNA LINC01234 in GC. Firstly, the usage of qRT‐PCR helped to establish expression pattern of LINC01234 in GC tissues. Following this, appropriate statistical tests were applied to analyze the relation between expression level and clinicopathological factors. Ultimately, potential functions and regulatory network of LINC01234 were concluded via GSEA and a series of bioinformatics tools or databases, respectively. Results Consequently, at the end of research we found LINC01234 is up‐regulated in GC tissues in comparison with adjacent normal tissues. Furthermore, its expression level is correlated with differentiation of patients with GC. It is also important to highlight bioinformatics analysis revealed that LINC01234 is involved in cancer‐associated pathways such as cell cycle and mismatch repair. Also, regulatory network of LINC01234 presented a probability in the involvement of tumorigenesis through regulating cancer‐associated genes. Conclusion Overall, our results suggested that LINC01234 may play a crucial role in GC.

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“…In serum specimens from patients with gastric cancer, dysregulation of miR-195-5p and miR-218-5p seems to indicate a poor prognosis, acting through the BIRC-r pathway [64]. Additionally, miR-1297 downregulation reportedly predicts poor prognosis in gastric cancer, via targeting of CREB1 [65]. Dysregulation of the miR-532/NCF2-NFkB feedback loop promotes gastric cancer angiogenesis and metastasis [66], and dysregulation of the miR-126/Crk protein axis predicts poor prognosis in gastric cancer [67].…”

Section: Prognostic Value Of Microrna In Gastric Tissue and Cancer Amentioning

confidence: 99%

Untitled

2020

Oncotarget

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Dysregulation of noncoding microRNA molecules has been associated with immune cell activation in the context of Helicobacter pylori induced gastric inflammation as well as carcinogenesis, but also with downregulation of mismatch repair genes, and may interfere with immune checkpoint proteins that lead to the overexpression of antigens on gastric tumor cells. Numerous miR-molecules have been described as important tools and markers in gastric inflammation and cancer development-including miR-21, miR-143, miR-145, miR-201, and miR-335-all of which are downregulated in gastric tumors, and involved in cell cycle growth or tumor invasion. Among the many microRNAs involved in gastric inflammation, adenocarcinoma development and immune checkpoint regulation, miR-155 is notable in that its upregulation is considered a key marker of chronic gastric inflammation that predisposes a patient to gastric carcinogenesis. Among various other miRs, miR-155 is highly expressed in activated B and T cells and in monocytes/macrophages present in chronic gastric inflammation. Notably, miR-155 was shown to downregulate the expression of certain MMR genes, such as MLH1, MSH2, and MSH6. In tumorinfiltrating miR-155-deficient CD8 + T cells, antibodies against immune checkpoint proteins restored the expression of several derepressed miR-155 targets, suggesting that miR-155 may regulate overlapping pathways to promote antitumor immunity. It may thus be of high clinical impact that gastric pathologies mediated by miR-155 result from its overexpression. This suggests that it may be possible to therapeutically attenuate miR-155 levels for gastric cancer treatment and/or to prevent the progression of chronic gastric inflammation into cancer. Research Perspective Oncotarget 895 www.oncotarget.com bead-based flow cytometric miRNA expression profiling method, they performed a systematic expression analysis of 217 mammalian miRNAs from 334 samples, including multiple human cancers. Their results demonstrated the general downregulation of miRNAs in tumors compared with normal tissues. Furthermore, they successfully identified poorly differentiated tumors based on miRNA expression profiles, whereas classification of the same samples using messenger RNA profiles was highly inaccurate. These findings highlight the potential of miRNA profiling for cancer diagnosis. Many miRNAs exhibit differential regulation in cancer-for example, miR-34a is involved in p53mediated apoptosis in pancreatic cancer, and nine miRNAs are upregulated in primary breast cancer, including miR-21, miR-181b, and miR-155 [2, 4, 5]. Zhang et al. (2008) reported that miR-21 plays a pivotal role in gastric cancer pathogenesis and progression, and Yan et al. obtained similar data in breast cancer [6]. Our own group has highlighted the distinctive roles of miR-375 and miR-133a for discriminating rectal and colon cancer, respectively, and has demonstrated significant downregulation of these molecules in CRC [7]. Interestingly, growth factor analysis reveals that IGF-2 expression may be as...

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Downregulation of MiR-1297 predicts poor prognosis and enhances gastric cancer cell growth by targeting CREB1

Cited by 27 publications

References 16 publications

<p>CREB1 Suppresses Transcription of microRNA-186 to Promote Growth, Invasion and Epithelial–Mesenchymal Transition of Gastric Cancer Cells Through the KRT8/HIF-1α Axis</p>

<p>CREB1 Suppresses Transcription of microRNA-186 to Promote Growth, Invasion and Epithelial–Mesenchymal Transition of Gastric Cancer Cells Through the KRT8/HIF-1α Axis</p>

Function and regulation annotation of up‐regulated long non‐coding RNA LINC01234 in gastric cancer

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