&lt;p&gt;Long non-coding RNA LINC00665 gastric cancer tumorigenesis by regulation miR-149-3p/RNF2 axis&lt;/p&gt;

Qi, Hongyang; Xiao, Zhanyu; Yun-xi, Wang

doi:10.2147/ott.s214588

Cited by 49 publications

(53 citation statements)

References 22 publications

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“…Similarly, in non-small-cell lung cancer (NSCLC) [ 16 ], LINC00665 expression is significantly upregulated and its silencing suppresses cell proliferation, induces apoptosis, and modulates the phosphoinositide 3-kinase/protein kinase B-signaling pathway. Additionally, we found that LINC00665 expression positively correlated with tumor size and TNM stage, but not with the age of patients; these results are consistent with earlier results related to gastric cancer [ 13 ], wherein LINC00665 expression correlated with the TNM stage and a poor patient prognosis. These results suggest that LINC00665 knockdown inhibits BC proliferation and invasion.…”

Section: Discussionsupporting

confidence: 92%

“…In contrast, LINC00665 knockdown inhibits cell proliferation and promotes apoptosis. In gastric cancer, LINC00665 expression is related to cancer staging and poor prognosis, and accelerates cell proliferation and invasion by binding miR-149-3p [ 13 ]. However, there is a paucity of scientific literature regarding the role of LINC00665 in BC.…”

Section: Introductionmentioning

confidence: 99%

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Knockdown of LINC00665 inhibits proliferation and invasion of breast cancer via competitive binding of miR-3619-5p and inhibition of catenin beta 1

Mao

et al. 2020

Cell Mol Biol Lett

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Background Long intergenic non-protein coding RNA00665 (LINC00665) plays a crucial tumorigenic role in many cancers, such as gastric cancer and lung adenocarcinoma. However, its role and mechanism of action in the progression of breast cancer (BC) are unknown. Methods LINC00665 expression levels were determined using quantitative polymerase chain reaction analysis with BC tissues and cell lines. BC cell proliferation was tested by performing 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assays, whereas BC cell migration and invasion capabilities were analyzed by performing transwell migration assays. Percentages of apoptotic cells were measured by flow cytometry. Interactions between LINC00665 and miR-3169-5p were examined by performing luciferase reporter assays, and the expression levels of proteins, such as β-catenin, were examined by western blot analysis. Results LINC00665 was expressed at high levels in BC tissues and cells. Upregulated LINC00665 expression correlated with tumor size and tumor, node, and metastasis stages, but not with the age of patients. LINC00665 knockdown inhibited BC cell proliferation, migration, and invasion, whereas it promoted apoptosis. Moreover, bioinformatics analysis and the luciferase reporter assay revealed that LINC00665 bound the microRNA (miR) miR-3619-5p. miR-3619-5p expression correlated negatively with LINC00665 expression in BC tissues. miR-3619-5p overexpression inhibited BC cell proliferation, migration, and invasion, but promoted apoptosis. Simultaneous knockdown of LINC00665 and miR-3619-5p led to increased cell proliferation, migration, and invasion, and inhibited apoptosis. Additionally, catenin beta 1, which encodes the β-catenin protein, was the target gene of miR-3619-5p. β-catenin expression clearly decreased after LINC00665 knockdown and miR-3619-5p overexpression, but increased after simultaneous knockdown of LINC00665 and miR-3619-5p. Conclusion LINC00665 knockdown inhibited BC cell proliferation and invasion by binding miR-3619-5p and inhibiting β-catenin expression.

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Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

Knockdown of LINC00665 inhibits proliferation and invasion of breast cancer via competitive binding of miR-3619-5p and inhibition of catenin beta 1

Mao

et al. 2020

Cell Mol Biol Lett

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“…12,13 LINC00665 has been reported to promote progression of several cancers, including lung cancer, gastric cancer and breast cancer. [14][15][16] Nevertheless, the functions and mechanism of LINC00665 in PC are unclear. We found that LINC00665 was highly expressed in prostate cancer tissues through bioinformatics analysis and qRT-PCR method.…”

Section: Introductionmentioning

confidence: 99%

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

Chen¹,

Yu²,

Huang³

et al. 2020

OTT

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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.

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“…LINC00665 can induce resistance to ge tinib via recruiting EZH2 and the activation of PI3K/AKT signaling in lung cancer [19]. LINC00665 can promote tumorigenesis of gastric cancer via regulating miR-149-3p and RNF2 [20]. In addition, LINC00665 contributes to breast cancer development via modulating miR-379-5p and LIN28B [21].…”

Section: Discussionmentioning

confidence: 99%

LINC00665 enhances tumorigenicity of endometrial carcinoma by interacting with high mobility group AT-hook 1

Liu

Chang

Cai

2020

Preprint

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Background: Endometrial carcinoma is a frequently diagnosed cancer among females. LncRNAs are reported to be associated with various cancers. Their biological roles in endometrial carcinoma progression is an emerging scientific area. LINC00665 can exert a significant role in many cancers. Up to now, its potential function in endometrial carcinoma is still poorly known.Method: qRT-PCR was carried out to test expression of LINC00665 and HMGA1. Western blot analysis was carried out to detect protein expression of HMGA1. Cell proliferation was evaluated using Cell Counting Kit-8 (CCK-8) and EdU assay. Flow cytometry assay was used to determine cell apoptosis and cell cycle. Would healing and transwell invasion assay was carried out to test cell migration and invasion. Immunohistochemical staining and HE staining were conducted to assess Ki-67 and tumor growth respectively.Results: Expression of LINC00665 in clinical endometrial carcinoma tissues and cells was obviously up-regulated. Loss of LINC00665 could repress endometrial carcinoma cell viability, induce cell apoptosis and blocked cell cycle in G1 phase. KLE and HHUA cell migration and invasion ability were depressed by LINC00665 shRNA. Decrease of LINC00665 suppressed endometrial carcinoma tumorigenicity in vivo. RIP assay evidenced LINC00665 directly bound with HMGA1 protein. shRNA of HMGA1 obviously restrained endometrial carcinoma cell growth and cell invasion.Conclusions: LINC00665 might promote endometrial carcinoma progression by positively modulating HMGA1.

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<p>Long non-coding RNA LINC00665 gastric cancer tumorigenesis by regulation miR-149-3p/RNF2 axis</p>

Cited by 49 publications

References 22 publications

Knockdown of LINC00665 inhibits proliferation and invasion of breast cancer via competitive binding of miR-3619-5p and inhibition of catenin beta 1

Knockdown of LINC00665 inhibits proliferation and invasion of breast cancer via competitive binding of miR-3619-5p and inhibition of catenin beta 1

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

LINC00665 enhances tumorigenicity of endometrial carcinoma by interacting with high mobility group AT-hook 1

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