miR-212 promotes pancreatic cancer cell growth and invasion by targeting the hedgehog signaling pathway receptor patched-1

Ma, Chao; Nong, Kate; Wu, Bo; Dong, Bo; Bai, Yuqiang; Zhu, Hongda; Wang, Weiwei; Huang, Xinyu; Zhang, Yuan; Ai, Kaixing

doi:10.1186/1756-9966-33-54

Cited by 86 publications

(68 citation statements)

References 29 publications

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“…Accumulating evidence demonstrate that miRNAs play important roles in a variety of biological processes and the deregulation of miRNAs is involved in many diseases [2,3]. Numerous studies have documented that miRNAs acted as oncogenes or tumor suppressors in diverse cancers, such as lung, breast, hepatic, pancreatic cancer and gastric cancer [4][5][6][7][8][9][10][11].…”

Section: Introductionmentioning

confidence: 99%

The role of microRNA-133b and its target gene FSCN1 in gastric cancer

Guo

Bai

Zou

et al. 2014

J Exp Clin Cancer Res

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Background: Increasing evidences have documented that microRNAs (miRNAs) act as oncogenes or tumor suppressors in gastric cancer (GC). In this study, we aimed to investigate the expression of miR-133b in a large number of GC samples and elucidate its role in GC carcinogenesis and the detailed mechanism. Methods: We used Taqman probe stem-loop real-time PCR to accurately measure the levels of miR-133b in 100 pairs of gastric cancer tissues and the adjacent non-neoplastic tissues. miR-133b mimics were overexpressed in GC cell lines, miR-133b inhibitors were also introduced in GES cells to investigate its role on regulating cell proliferation, cell migration and cell invasion. The target of miR-133b was identified by luciferase reporter assay and western blot. Fascin actin-bundling protein 1 (FSCN1) siRNA was used to achieve the knockdown of FSCN1 in GC cells and to investigate its role on modulating GC cell proliferation and invasion. Results: miR-133b was significantly down-regulated in GC cell lines and in GC tissues compared with adjacent normal tissues. Moreover, lower-level of miR-133b was also associated with venous invasion and a more aggressive tumor phenotype. Re-introduction of miR-133b in GC cells can inhibit cell proliferation, cell migration and invasion. In contrary, knockdown of miR-133b in GES cells can promote cell proliferation and invasion. Further investigation indicated that miR-133b targeted FSCN1 in GC cells and knockdown of FSCN1 can also inhibit GC cell growth and invasion. Conclusion: Our findings demonstrated that miR-133b was significantly down-regulated in GC tissues and exerted its tumor suppressor role in GC cells. The investigation of the detailed mechanism showed that miR-133b directly targeted FSCN1 which functioned as an oncogenic gene in GC cells. These results suggested that miR-133b can be developed as a new diagnostic marker or therapeutic target for GC.

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Section: Introductionmentioning

confidence: 99%

The role of microRNA-133b and its target gene FSCN1 in gastric cancer

Guo

Bai

Zou

et al. 2014

J Exp Clin Cancer Res

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“…Other studies have also demonstrated the key function of miR-212-3p in pancreatic cancer metastasis; Park et al (22) demonstrated that miR-212 expression increased in pancreatic cancer cells and promoted their proliferation by inhibiting Retinoblastoma 1 gene expression in a targeted manner. In addition, Ma et al (23) demonstrated that miR-212 promoted tumor cell proliferation and infiltration by the targeted inhibition ofPatch-1 gene expression. Data from the present study confirmed that IFN-γ could inhibit miR-212-3p expression in pancreatic cancer cells, and thus upregulate the expression of RFXAP and MHC class II.…”

Section: Discussionmentioning

confidence: 99%

IFN-γ induces the upregulation of RFXAP via inhibition of miR-212-3p in pancreatic cancer cells: A novel mechanism for IFN-γ response

et al. 2018

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Abstract. Previous studies have demonstrated that pancreatic cancer-derived microRNA (miR)-212-3p can inhibit the expression of regulatory factor X-associated protein (RFXAP), an important transcription factor for major histocompatibility complex (MHC) class II, and thereby lead to downregulation of MHC class II in dendritic cells. It has also been established that interferon (IFN)-γ can increase the expression of MHC class II in immune cells. It was therefore hypothesized that IFN-γ can inhibit miR-212-3p expression in pancreatic cancer, leading to the upregulation of RFXAP and MHC class II expression. This may represent a novel molecular mechanism underlying the use of IFN-γ in immunotherapy. Data from the present study revealed that miR-212-3p was inhibited by IFN-γ in a dose and time-dependent manner in the pancreatic ductal adenocarcinoma cell line PANC-1. RFXAP and MHC class II expression were increased following IFN-γ stimulation. A luciferase assay was performed to validate RFXAP as a target gene of miR-212-3p. The expression levels of RFXAP and MHC class II were decreased by miR-212-3p mimics and increased by miR-212-3p inhibitors. In PANC-1 cells transfected with miR-212-3p mimics, IFN-γ stimulation could not increase the RFXAP and MHC class II. The results from the present study suggest that IFN-γ increases RFXAP and MHC class II expression by inhibiting miR-212-3p. To the best of our knowledge, this is the first report of this novel molecular mechanism underlying the effects of IFN-γ on pancreatic cancer, which may aid with the development of immunotherapies for patients with pancreatic cancer.

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“…Various miRNAs, such as miR-200 [7], miR-146a [8], miR-486 [9], and let-7 family [10] have been confirmed to be tumor suppressors. Meanwhile, PDAC malignancy was found to be positively associated with miR-196a [11], miR-212 [12], and miR-31 [13]. We chose to focus on miR-140 because it is closely related to many different malignancies, such as mastocarcinoma [14], colorectal carcinoma [15], liver cancer [16], and osteosarcoma [17].…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-140 regulates cell growth and invasion in pancreatic duct adenocarcinoma by targeting iASPP

Liang

Gong

Zhang

et al. 2016

ABBS

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MicroRNAs are ∼22 nucleotide RNAs processed from RNA hairpin structures that play important roles in regulating protein expression level via binding to mRNA, either suppressing its translation or speeding up its degradation. In humans, they regulate most protein-coding genes, including genes important in cancer and other diseases. In this study, the expression of microRNA-140 (miR-140) was demonstrated to be significantly suppressed in pancreatic duct adenocarcinoma specimens and cell lines, compared with their adjacent normal tissues. With the help of bioinformatics analysis, inhibitor of apoptosis-stimulating protein of p53 (iASPP) was identified to be a direct target of miR-140, and luciferase reporter experiment confirmed this discovery. Overexpression of miR-140 decreases the protein expressions of iASPP, ΔNp63, MMP2, and MMP9. Growth and invasion of PANC-1 cells were attenuated by overexpression of miR-140 in vitro. The suppressive effect of miR-140 on PANC-1 cell line could be partly balanced out by manual overexpression of iASPP. Above all, these findings provided insights into the functional mechanism of miR-140, suggested that the miR-140/iASPP axis may interfere with the proliferative and invasive property of pancreatic duct adenocarcinoma cells, and indicated that miR-140 could be a potential therapeutic target for pancreatic duct adenocarcinoma.

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miR-212 promotes pancreatic cancer cell growth and invasion by targeting the hedgehog signaling pathway receptor patched-1

Cited by 86 publications

References 29 publications

The role of microRNA-133b and its target gene FSCN1 in gastric cancer

The role of microRNA-133b and its target gene FSCN1 in gastric cancer

IFN-γ induces the upregulation of RFXAP via inhibition of miR-212-3p in pancreatic cancer cells: A novel mechanism for IFN-γ response

MicroRNA-140 regulates cell growth and invasion in pancreatic duct adenocarcinoma by targeting iASPP

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