&lt;p&gt;lncRNA SLCO4A1-AS1 promotes growth and invasion of bladder cancer through sponging miR-335-5p to upregulate OCT4&lt;/p&gt;

Yu, Yang; Wang, Feng; Huang, Hang; Zhang, Yan; Xie, Hui; Men, Tongyi

doi:10.2147/ott.s191740

Cited by 35 publications

(43 citation statements)

References 32 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…30 LncRNA SLCO4A1-AS1 contributes to bladder cancer progression by inhibiting miR-335-5p. 31 LncRNA PVT1 facilitates bladder cancer development by sponging miR-143. 32 Thus, we analyzed the potential targets of LINC00665.…”

Section: Dovepressmentioning

confidence: 99%

<p>LncRNA LINC00665 Promotes Prostate Cancer Progression via miR-1224-5p/SND1 Axis</p>

Chen¹,

Yu²,

Huang³

et al. 2020

OTT

Self Cite

View full text Add to dashboard Cite

Background: Increasing researches have revealed a critical role of long noncoding RNAs (lncRNAs) in tumor progression. LINC00665 is a poorly investigated lncRNA. In this research, we sought to determine the potential role of LINC00665 in prostate cancer (PC) progression. Methods: LINC00665 expression was analyzed by bioinformatics method and qRT-PCR. Proliferation was determined via CCK8 and colony formation assays. Transwell assay was conducted to analyze migration and invasion. Xenograft assay was used to test the roles of LINC00665 in vivo. Luciferase reporter assay, pulldown assay and RIP assay were utilized to confirm the interaction between LINC00665 and miR-1224-5p. Results: LINC00665 expression was increased in PC samples in contrast to control tissues, according to bioinformatics analysis and qRT-PCR validation. LINC00665 high expression was related to a poor prognosis. LINC00665 knockdown markedly attenuated growth and metastasis of PC cells and impaired tumor propagation in vivo. Mechanistic investigation revealed that LINC00665 was the sponge for miR-1224-5p. By inhibiting miR-1224-5p level, LINC00665 dramatically promoted the expression of SND1 in PC cells. Ectopic expression of SND1 significantly rescued the effects of LINC00665 silencing. Conclusion: LINC00665 is a novel oncogenic gene in PC by targeting miR-1224-5p/SND1 pathway and may be a therapeutic target.

show abstract

Section: Dovepressmentioning

confidence: 99%

<p>LncRNA LINC00665 Promotes Prostate Cancer Progression via miR-1224-5p/SND1 Axis</p>

Chen¹,

Yu²,

Huang³

et al. 2020

OTT

Self Cite

View full text Add to dashboard Cite

show abstract

“… 3 - 5 Despite clinical advances in surgical surgery, radiation therapy, immunotherapy, chemotherapy, or combined therapies, the 5-year survival rate of BC remains bleak. 6 , 7 Tumor invasion and metastasis are still the major causes of treatment failure and patient death. Therefore, it is urgent to investigate the potential molecular mechanisms involved in metastatic BC progression.…”

Section: Introductionmentioning

confidence: 99%

Overexpression of DDR1 Promotes Migration, Invasion, Though EMT-Related Molecule Expression and COL4A1/DDR1/MMP-2 Signaling Axis

Xie

Zhang

et al. 2020

Technol Cancer Res Treat

View full text Add to dashboard Cite

Purpose: Discoidin domain receptor 1 (DDR1) belongs to a novel class of receptor tyrosine kinases. Previous evidence indicates that DDR1 overexpression promotes the aggressive growth of bladder cancer (BC) cells. This study aimed to investigate the molecular mechanisms by which DDR1 influences BC. Methods: DDR1 was transfected into human BC RT4 cells. DDR1, COL4A1, and MMP-2 expression in 30 BC tissues and paired adjacent tissues were examined by real-time polymerase chain reaction (RT-PCR) and immunohistochemistry. Transwell assays were conducted to determine cell migration and invasion. RT-PCR and western blot (WB) were also used to measure the DDR1, COL4A1, MMP-2, and EMT-related gene (ZEB1 and SLUG) expression in RT4 cells after DDR1 overexpression. Results: COL4A1 and MMP-2 interacted with DDR1 in the PPI network. RT-PCR and immunohistochemistry results showed that both mRNA and protein levels of DDR1 and COL4A1 were significantly increased in BC tissue, while the expression of MMP-2 was increased only at the mRNA level ( P < 0.05). Overexpression of DDR1 in RT4 cells significantly promoted their migratory and invasive capabilities in vitro ( P < 0.05). Moreover, overexpression of DDR1 in RT4 cells increased the mRNA and protein expression of ZEB1, SLUG, COL4A1, and MMP-2 ( P < 0.01). DDR1-mediated migration and invasion of RT4 cells were reversed after COL4A1-siRNA treatment. Conclusion: DDR1 may be a potential therapeutic target in BC patients.

show abstract

“…For example, long noncoding RNA CASC2 upregulates PTEN to suppress pancreatic adenocarcinoma metastasis by downregulating miR-21 8 . LncRNA SLCO4A1-AS1 promotes growth and invasion of bladder cancer through sponging miR-335-5p to upregulate OCT4 9 . LncRNA LINC00460 promoted colorectal cancer cells metastasis via sponging miR-939-5p 10 .…”

Section: Introductionmentioning

confidence: 99%

LINC01232 exerts oncogenic activities in pancreatic adenocarcinoma via regulation of TM9SF2

Lei

et al. 2019

Cell Death Dis

View full text Add to dashboard Cite

Pancreatic adenocarcinoma (PAAD), one of the most prevailing malignant tumors in digestive system, is identified as one of the main culprits of cancer-associated mortality. Despite long intergenic non-protein coding RNA 1232 (LINC01232) is found to be upregulated in TCGA PAAD tissues and associated with poor prognosis, the potential of LINC01232 in PAAD progression still needs more explorations. In this study, LINC01232 was chosen to be the research object in PAAD cellular processes. Functionally, loss-of function assays were carried out and the experimental results indicated that suppression of LINC01232 hindered the deterioration of PAAD by affecting cell proliferation and migration. Furthermore, relationship between LINC01232 and its nearby gene transmembrane 9 superfamily member 2 (TM9SF2) was investigated. The same expression pattern of TM9SF2 in TCGA PAAD samples was observed. It was found that upregulation of LINC01232 could be a crucial factor for the dysregulation of TM9SF2. Mechanistically, LINC01232 recruited EIF4A3 to boost TM9SF2 mRNA stability. Besides, our findings demonstrated that the transcriptional activation of LINC01232 and TM9SF2 was mediated by SP1. Therefore, we concluded that LINC01232 executed carcinogenic properties in PAAD progression via regulation of TM9SF2. In conclusion, this study was the first to unveil the role and molecular mechanism of LINC01232, suggesting LINC01232 as a promising molecular target for pancreatic cancer treatment.

show abstract

<p>lncRNA SLCO4A1-AS1 promotes growth and invasion of bladder cancer through sponging miR-335-5p to upregulate OCT4</p>

Cited by 35 publications

References 32 publications

<p>LncRNA LINC00665 Promotes Prostate Cancer Progression via miR-1224-5p/SND1 Axis</p>

<p>LncRNA LINC00665 Promotes Prostate Cancer Progression via miR-1224-5p/SND1 Axis</p>

Overexpression of DDR1 Promotes Migration, Invasion, Though EMT-Related Molecule Expression and COL4A1/DDR1/MMP-2 Signaling Axis

LINC01232 exerts oncogenic activities in pancreatic adenocarcinoma via regulation of TM9SF2

Contact Info

Product

Resources

About