MicroRNA‑144 mediates chronic inflammation and tumorigenesis in colorectal cancer progression via regulating C‑X‑C motif chemokine ligand 11

Han, Bin; Feng, Dan; Yu, Xin; Liu, Yuanqi; Yang, Ming; Luo, Fei; Zhou, Liming; Fu, Liu

doi:10.3892/etm.2018.6389

Cited by 10 publications

(9 citation statements)

References 36 publications

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“…For example, miR-144 has been identified as a tumor suppressive miRNA in multiple types of cancers, such as gastric cancer (Mushtaq et al, 2019), lung cancer (Jiang et al, 2019), cervical cancer , and colorectal cancer (Sheng et al, 2019). Specifically, miR-144 was down-regulated in colorectal cancer cells and tissues, and suppressed cancer development by directly targeting SMAD4 (Sheng et al, 2019) and CXCL11 (Han et al, 2018). Furthermore, miR-144 expression was lower in primary human osteosarcoma tissue samples and osteosarcoma cell lines (Zhao et al, 2014).…”

Section: Discussionmentioning

confidence: 99%

Long Non-coding RNA SNHG17 Promotes Cell Proliferation and Invasion in Castration-Resistant Prostate Cancer by Targeting the miR-144/CD51 Axis

et al. 2020

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Previously, we found that the expression of long non-coding RNA (lncRNA) small nucleolar RNA host gene 17 (SNHG17) was up-regulated in castration-resistant prostate cancer (CRPC) cells compared to that in hormone sensitive prostate cancer (HSPC) cells. Moreover, we found that CD51 was up-regulated in prostate cancer cells and promoted the carcinogenesis and progression of prostate cancer. However, the regulatory mechanism of SNHG17 and CD51 in the development of CRPC remains unclear. In the current study, we aimed to elucidate the expressions, functions, and underlying mechanism of SNHG17 and CD51 in CRPC. Our results further confirmed that both SNHG17 and CD51 were up-regulated in CRPC tissues and cells. In addition, we found that SNHG17 expression was positively correlated with CD51 expression in prostate cancer. Mechanically, SNHG17 functioned as a competing endogenous RNA (ceRNA) to up-regulate CD51 expression through competitively sponging microRNA-144 (miR-144), and CD51 was identified as a direct downstream target of miR-144 in CRPC. Functionally, down-regulation of SNHG17 or up-regulation of miR-144 inhibited the proliferation, migration, and invasion of CRPC cells, whereas up-regulation of SNHG17 and down-regulation of miR-144 promoted the proliferation, migration and invasion of CRPC cells in vitro and in vivo. Using gain and loss-of function assay and rescue assay, we showed that miR-144 inhibited cell proliferation, migration and invasion by directly inhibiting CD51 expression, and SNHG17 promoted cell proliferation, migration and invasion by directly enhancing CD51 expression in CRPC cells. Taken together, our study reveals the role of the SNHG17/miR-144/CD51 axis in accelerating CRPC cell proliferation and invasion, and suggests that SNHG17 may serve as a novel therapeutic target for CRPC.

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Section: Discussionmentioning

confidence: 99%

Long Non-coding RNA SNHG17 Promotes Cell Proliferation and Invasion in Castration-Resistant Prostate Cancer by Targeting the miR-144/CD51 Axis

et al. 2020

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“…CXCL11 was significantly upregulated in CRC tissues, while miR-144 was downregulated. The upregulation of miR-144 via the downregulation of CXCL11 leads to the inhibition of inflammation and tumorigenesis [76]. The mTOR is a serine/threonine kinase that is involved in several biological processes, such as cellular growth, metabolism, and cytoskeleton regulation.…”

Section: Mir-144 In Colorectal Cancermentioning

confidence: 99%

MiR-144: A New Possible Therapeutic Target and Diagnostic/Prognostic Tool in Cancers

Kooshkaki

Rezaei

Rahmati

et al. 2020

IJMS

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MicroRNAs (miRNAs) are small and non-coding RNAs that display aberrant expression in the tissue and plasma of cancer patients when tested in comparison to healthy individuals. In past decades, research data proposed that miRNAs could be diagnostic and prognostic biomarkers in cancer patients. It has been confirmed that miRNAs can act either as oncogenes by silencing tumor inhibitors or as tumor suppressors by targeting oncoproteins. MiR-144s are located in the chromosomal region 17q11.2, which is subject to significant damage in many types of cancers. In this review, we assess the involvement of miR-144s in several cancer types by illustrating the possible target genes that are related to each cancer, and we also briefly describe the clinical applications of miR-144s as a diagnostic and prognostic tool in cancers.Int. J. Mol. Sci. 2020, 21, 2578 2 of 23 of a mRNA molecule [3]. MiRNAs indicate a new perspective in the study of cancers. More than 50% of miRNA genes were discovered to be located within the genomic regions that are involved in cancers, suggesting their role in human cancer pathogenesis. In pathological conditions, MiRNAs can negatively regulate gene expression and they are associated with tumor growth, apoptosis, invasion, and metastasis. In the past, several studies have indicated the ability of miRNAs in the inhibition of tumors as a critical option for the improvement of cancer therapy [4,5]. Tumor activator miRNAs, called oncomiRs, are overexpressed in various cancers. On the contrary, suppressive tumor miRNAs are underexpressed [6][7][8]. Among several miRNAs assessed, miR-144s seem to have a role in several cancers. These miRNAs are located in the chromosomal region 17q11.2, being significantly destroyed in many types of cancers. The predicted stem-loop structure of miR-144s recognized by the miRBase (http://mirbase.org/) is shown in Figure 1A. The miR-144 hairpin gives rise to the "guide strand" miR-144-5p and the sister "passenger" strand miR-144-3p ( Figure 1B).

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“…CXCL9 and CXCL11 belong to the chemokine CXC family, and may be induced by interferon-γ, which is associated with the regulation of immune cells (26,27). Previous studies have indicated that CXCL9 and CXCL11 were overexpressed and functioned as tumour suppressors in several types of cancer, including ovarian cancer (28), breast cancer (29), lung cancer (30), prostate cancer (27), gastric cancer (31), lymphoma (32) and colorectal cancer (33). Recent studies have also indicated that CXCL9/11 upregulates the expression of PD-L1, suggesting that CXCL9/11 may be factors influencing the effects of immunotherapy (31).…”

Section: Discussionmentioning

confidence: 99%

Identification of key candidate genes and pathways in oral squamous cell carcinoma by integrated Bioinformatics analysis

Zou

et al. 2019

Exp Ther Med

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Oral squamous cell carcinoma (OSCC) is one of the most common types of malignant head and neck tumor, which poses a serious threat to human health. In recent years, the incidence of OSCC has been increasing, while the prognosis has not significantly improved. Elucidation of the molecular mechanisms underlying the development of OSCC may provide novel therapeutic strategies. In the present study, the gene expression profiles from 4 datasets, including 244 OSCC and 95 normal oral mucosa samples, were subjected to statistical and Bioinformatics analysis. A total of 34 differentially expressed genes (DEGs) were identified, among which 14 were upregulated and 20 were downregulated in OSCC compared with normal oral mucosa tissues. Gene Ontology enrichment analysis indicated that the DEGs were mainly involved in regulation of the immune response, cell adhesion and cell proliferative processes. The Kyoto Encyclopedia of Genes and Genomes pathway analysis revealed that the DEGs were mainly associated with the phosphoinositide-3 kinase Akt and Toll-like receptor signaling pathway. The key candidate DEGs were identified from the complex protein-protein interaction network, and secreted phosphoprotein 1 (SPP1), integrin subunit α 3 and plasminogen activator, urokinase (PLAU) were confirmed to be significantly associated with the survival rate. Cell Counting Kit-8 and Transwell assays demonstrated that SPP1 and PLAU regulate cell proliferation, migration and invasion. The candidate genes/pathways identified in the present study may include promising diagnostic biomarkers or therapeutic targets for OSCC.

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MicroRNA‑144 mediates chronic inflammation and tumorigenesis in colorectal cancer progression via regulating C‑X‑C motif chemokine ligand 11

Cited by 10 publications

References 36 publications

Long Non-coding RNA SNHG17 Promotes Cell Proliferation and Invasion in Castration-Resistant Prostate Cancer by Targeting the miR-144/CD51 Axis

Long Non-coding RNA SNHG17 Promotes Cell Proliferation and Invasion in Castration-Resistant Prostate Cancer by Targeting the miR-144/CD51 Axis

MiR-144: A New Possible Therapeutic Target and Diagnostic/Prognostic Tool in Cancers

Identification of key candidate genes and pathways in oral squamous cell carcinoma by integrated Bioinformatics analysis

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