Involvement of the MicroRNA-1-LITAF Axis in Gastric Cancer Cell Growth and Invasion

Chen, Yen-Chih; Wu, Chung Chih; Tu, Yating; Chen, Yi-Ru; Lee, Ming‐Cheng

doi:10.21873/anticanres.14645

Cited by 7 publications

(5 citation statements)

References 37 publications

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“…To further investigate more mechanisms of REEP6 for its biological roles, we also predicted the interaction network of REEP6 using the Search Tool for the Retrieval of Interacting Genes/Proteins (STRING) database, and we found that REEP6 was associated with Atlastin GTPase 2 (ATL2), ATL3, killer cell lectin-like receptor F1 [40], nucleoredoxin-like 2 [41], reticulon 1-4 [42][43][44], sorting nexin 15 [45], transmembrane protein 33 (TMEM33) [46] and lipopolysaccharide induced TNF factor (LITAF) [47,48] (Figure S3), and these partners of REEP6 were reported to be associated with cancer progression. For example, REEP6 might regulate the expression and transport of TMEM33 to promote the cell proliferation of TSCC [46].…”

Section: Discussionmentioning

confidence: 99%

“…For example, REEP6 might regulate the expression and transport of TMEM33 to promote the cell proliferation of TSCC [46]. Moreover, REEP6 might also regulate LITAF for inducing cancer growth/invasion [47] or switching tumor associated-inflammation [48]. According to the prediction, further studies would be needed to investigate whether REEP6 regulates the malignancy of TSCC through the predicted interaction network.…”

Section: Discussionmentioning

confidence: 99%

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The Clinical and Biological Effects of Receptor Expression-Enhancing Protein 6 in Tongue Squamous Cell Carcinoma

et al. 2023

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There are currently no effective biomarkers for the diagnosis and treatment of tongue squamous cell carcinoma (TSCC), which causes a poor 5-year overall survival rate. Thus, it is crucial to identify more effective diagnostic/prognostic biomarkers and therapeutic targets for TSCC patients. The receptor expression-enhancing protein 6 (REEP6), a transmembrane endoplasmic reticulum resident protein, controls the expression or transport of a subset of proteins or receptors. Although it was reported that REEP6 plays a role in lung and colon cancers, its clinical impact and biological role in TSCC are still unknown. The present study aimed to identify a novel effective biomarker and therapeutic target for TSCC patients. Expression levels of REEP6 in specimens from TSCC patients were determined with immunohistochemistry. Gene knockdown was used to evaluate the effects of REEP6 in cancer malignancy (colony/tumorsphere formation, cell cycle regulation, migration, drug resistance and cancer stemness) of TSCC cells. The clinical impact of REEP6 expression and gene co-expression on prognosis were analyzed in oral cancer patients including TSCC patients from The Cancer Genome Atlas database. Tumor tissues had higher levels of REEP6 compared to normal tissues in TSCC patients. Higher REEP6 expression was related to shorter disease-free survival (DFS) in oral cancer patients with poorly differentiated tumor cells. REEP6-knocked-down TSCC cells showed diminished colony/tumorsphere formation, and they also caused G1 arrest and decreased migration, drug resistance and cancer stemness. A high co-expression of REEP6/epithelial–mesenchymal transition or cancer stemness markers also resulted in poor DFS in oral cancer patients. Thus, REEP6 is involved in the malignancy of TSCC and might serve as a potential diagnostic/prognostic biomarker and therapeutic target for TSCC patients.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

The Clinical and Biological Effects of Receptor Expression-Enhancing Protein 6 in Tongue Squamous Cell Carcinoma

et al. 2023

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“…According to the manufacturer's instructions (Invitrogen, Carlsbad, CA, USA) and as we described previously [34], total RNA was reverse transcribed through a stem-loop reverse transcription reaction by using miR-1-3p reverse transcription primers (5 -CTCAACTGGTGTCGTGGAGTCGG CAATTCAGTTGAGATACATAC-3 ) and SuperScript III Reverse Transcriptase. Gene expression was assessed using an SYBR Green I assay (Applied Biosystems) and the expression level of miR-1-3p was normalized to that of U6 (∆Ct = miR-1-3p Ct-U6 Ct).…”

Section: Stem-loop Reverse Transcription Pcrmentioning

confidence: 99%

“…After 24 h of transfection, the luciferase activity was examined using the Dual-Glo Luciferase Assay System (Promega Corporation, Madison, WI, USA). The detailed information was described in our previous study [34].…”

Section: Mirna Target Candidates and Luciferase Reporter Assaymentioning

confidence: 99%

Involvement of MicroRNA-1-FAM83A Axis Dysfunction in the Growth and Motility of Lung Cancer Cells

Liu

Chen

Yeah

et al. 2020

IJMS

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Lung cancer is the most prevalent types of cancer and the leading cause of cancer-related deaths worldwide. Among all cancers, lung cancer has the highest incidence, accompanied by a high mortality rate at the advanced stage. Favorable prognostic biomarkers can effectively increase the survival rate in lung cancer. Our results revealed FAM83A (Family with sequence similarity 83, member A) overexpression in lung cancer tissues compared with adjacent normal tissues. Furthermore, high FAM83A expression was closely associated with poor lung cancer survival. Here, through siRNA transfection, we effectively inhibited FAM83A expression in the lung cancer cell lines H1355 and A549. FAM83A knockdown significantly suppressed the proliferation, migration, and invasion ability of these cells. Furthermore, FAM83A knockdown could suppress Epidermal growth factor receptor (EGFR)/Mitogen-activated protein kinase (MAPK)/Choline kinase alpha (CHKA) signaling activation in A549 and H1355. By using a bioinformatics approach, we found that FAM83A overexpression in lung cancer may result from miR-1-3p downregulation. In summary, we identified a novel miR-1-FAM83A axis could partially modulate the EGFR/choline phospholipid metabolism signaling pathway, which suppressed lung cancer growth and motility. Our findings provide new insights for the development of lung cancer therapeutics.

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“…Moreover, it has been identified that miR-1-3p participated in the occurrence and development of multiple tumor diseases, like prostate cancer (Li et al 2018), non-small-cell lung cancer (Wang et al 2019a, b), hepatocellular carcinoma ) and so on. Especially, Ke et al (Ke et al 2019) and Chen et al (Chen et al 2020) suggested that miR-1-3p inhibited gastric cancer cell growth and metastasis. To further find out the upstream regulation mechanism of miR-1-3p, the supposed binding sequence between LINC00242 and miR-1-3p was predicted.…”

Section: Introductionmentioning

confidence: 99%

LINC00242/miR-1-3p/G6PD axis regulates Warburg effect and affects gastric cancer proliferation and apoptosis

Deng

et al. 2021

Mol Med

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Background Reprogrammed glucose metabolism of enhanced Warburg effect (or aerobic glycolysis) is considered as a hallmark of cancer. Long non-coding RNAs (lncRNAs) have been certified to play a crucial role in tumor progression. The current study aims to inquire into the potential regulatory mechanism of long intergenic non-protein coding RNA 242 (LINC00242) on aerobic glycolysis in gastric cancer. Method LINC00242, miR-1-3p and G6PD expression levels in gastric cancer tissues and cells were determined by qRT-PCR. Cell apoptosis or viability were examined by Flow cytometry or MTT assay. Western blot was utilized to investigate G6PD protein expression levels. Immunohistochemical (IHC) and hematoxylin and eosin (H&E) staining were used for histopathological detection. The targeted relationship between LINC00242 or G6PD and miR-1-3p was verified by luciferase reporter gene assay. Nude mouse xenograft was utilized to detect tumor formation in vivo. Result LINC00242 and G6PD was high-expressed in gastric cancer tissues and cells, and LINC00242 is positively correlated with G6PD. Silencing of LINC00242 or G6PD within gastric cancer cells prominently inhibited cell proliferation and aerobic glycolysis in vitro and relieved the tumorigenesis of gastric cancer in vivo. miR-1-3p was predicted to directly target both LINC00242 and G6PD. Overexpression of miR-1-3p suppressed gastric cancer cells proliferation and aerobic glycolysis. LINC00242 competitively combined miR-1-3p, therefore relieving miR-1-3p-mediated suppression on G6PD. Conclusion LINC00242 plays a stimulative role in gastric cancer aerobic glycolysis via regulation of miR-1-3p/ G6PD axis, therefore affecting gastric cancer cell proliferation.

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Involvement of the MicroRNA-1-LITAF Axis in Gastric Cancer Cell Growth and Invasion

Cited by 7 publications

References 37 publications

The Clinical and Biological Effects of Receptor Expression-Enhancing Protein 6 in Tongue Squamous Cell Carcinoma

The Clinical and Biological Effects of Receptor Expression-Enhancing Protein 6 in Tongue Squamous Cell Carcinoma

Involvement of MicroRNA-1-FAM83A Axis Dysfunction in the Growth and Motility of Lung Cancer Cells

LINC00242/miR-1-3p/G6PD axis regulates Warburg effect and affects gastric cancer proliferation and apoptosis

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