Long non-coding RNA TUG1 mediates 5-fluorouracil resistance by acting as a ceRNA of miR-197-3p in colorectal cancer

Wang, Meng; Hu, Hanqing; Wang, Yuliuming; Huang, Quanlong; Huang, Rui; Chen, Yinggang; Ma, Tianyi; Qiao, Tianyu; Zhang, Qian; H, Wu; Chen, Qingmin; Han, Dong; Wang, Guiyu; Wang, Xishan

doi:10.7150/jca.32065

Cited by 61 publications

(39 citation statements)

References 37 publications

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“…There is increasing evidence that a high lncRNA expression is significantly correlated with unfavorable CRC prognosis. The elevated expressions of lncRNA TTN-AS1, XIST, TUG1, and SNHG12 indicate poor prognoses for CRC patients (Liu et al, 2018;Liu Y. et al, 2019;Wang M. et al, 2019;. Our multivariate survival study proved that LINC00115 is an independent prognostic factor for relapse and poor survival in CRC patients.…”

Section: Discussionmentioning

confidence: 54%

Long Non-coding RNA LINC00115 Contributes to the Progression of Colorectal Cancer by Targeting miR-489-3p via the PI3K/AKT/mTOR Pathway

Feng

Wang

et al. 2020

Front. Genet.

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Long non-coding RNAs (lncRNAs) are tumor-related regulators and have been found to be involved in the underlying molecular mechanisms of colorectal cancer (CRC). However, the role of lncRNA LINC00115 during CRC progression is not entirely elucidated. In this study, we discovered that LINC00115 was significantly overexpressed in CRC, and its overexpression predicted poor patient outcomes. Downregulation of LINC00115 markedly inhibited CRC cell proliferation, increased cell apoptosis, and suppressed cell migration and invasion. Moreover, downregulation of LINC00115 led to the inactivation of PI3K/AKT/mTOR signaling. Bioinformatics analysis identified miR-489-3p as a candidate target of LINC00115. Furthermore, we revealed an inverse correlation between LINC00115 and miR-489-3p in CRC tissues. Importantly, by luciferase reporter assay, we found that miR-489-3p might directly target LINC00115, and downregulation of miR-489-3p could rescue the biological effects induced by the absence of LINC0015. In conclusion, our findings demonstrated that LINC00115 serves as an oncogene in CRC metastasis. Deeper understanding of the LINC00115/miR-489-3p axis might provide potential therapeutic targets against CRC metastasis.

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Section: Discussionmentioning

confidence: 54%

Long Non-coding RNA LINC00115 Contributes to the Progression of Colorectal Cancer by Targeting miR-489-3p via the PI3K/AKT/mTOR Pathway

Feng

Wang

et al. 2020

Front. Genet.

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“…15 However, nearly 50% of colorectal cancer patients showed no response to 5-Fu, and more and more studies reported that fluorouracil resistance led to failure of CRC treatment. [16][17][18] But the mechanism is not clear. Therefore, biomarkers predicting the efficacy of fluorouracil are urgently needed in CRC treatment.…”

Section: Introductionmentioning

confidence: 99%

<p>Inhibition of CDK1 Reverses the Resistance of 5-Fu in Colorectal Cancer</p>

Zhu

Zhang

et al. 2020

CMAR

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Introduction: Although the survival rate of colorectal cancer (CRC) patients can be improved by surgery, radiotherapy, and chemotherapy, the resistance to 5-fluorouracil (5-Fu) affects the effect of chemotherapy and the prognosis of patients. An increasing number of studies showed that 5-Fu resistance was the main reason for the failure of colorectal cancer treatment. The poor prognosis of colorectal cancer greatly harms people's health. This study aimed to clarify the correlation between cyclin-dependent kinase 1 (CDK1) and 5-Fu-induced tumor resistance. Materials and Methods: Cell proliferation and invasion experiments showed that downregulation of CDK1 inhibited fluorouracil-resistant CRC cell proliferation. The expression level of CDK1 was detected in 5-Fu-resistant CRC cells in vitro. Tumor growth was inhibited by down-regulation of CDK1 in tumor xenograft mouse models. Results: We found that CDK1 was highly expressed in tumor tissues, especially in fluorouracil-resistant tissues. We also confirmed that the differential expression of 5-Fu in tumor tissues was related to tumor site, lymph node metastasis and stage. CDK1 promoted migration, invasion and inhibited apoptosis in 5-Fu-resistant CRC cells. Down-regulation of CDK1 inhibited fluorouracil-resistant CRC cell proliferation and tumorigenesis in vivo. Conclusion: High expression of CDK1 may lead to poor clinical prognosis, and inhibition of CDK1 enhances 5-Fu sensitivity in CRC. Our research suggested that CDK1 may be used to predict 5-Fu efficacy and as a therapeutic target for CRC.

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“…There is increasing evidence that a high lncRNA expression is signi cantly correlated with unfavorable CRC prognosis. The elevated expressions of lncRNA TTN-AS1, XIST, TUG1 and SNHG12 indicate poorer prognoses of CRC patients [17,[22][23][24]. Our multivariate survival study proved that LINC00115 are independent prognostic factors for poor relapse-survival in CRC patients.…”

Section: Discussionmentioning

confidence: 54%

Long non-coding RNA LINC00115 contributes to the progression of colorectal cancer by targeting miR-489-3p via PI3K/AKT/mTOR pathway

Feng

Wang

et al. 2020

Preprint

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Background Long noncoding RNAs (lncRNAs) are tumor-related regulators and have been found to be involved in the underlying molecular mechanisms of colorectal cancer (CRC). However, the role of lncRNA LINC00115 during CRC progression is not entirely elucidated. Methods The expression of LINC00115 was analyzed in paired CRC tissue samples and its clinical significance was evaluated. The biological effects on CRC cells proliferation, apoptosis, migration, invasion and PI3K/AKT/mTOR signaling were assessed by Cell Counting Kit-8 assay, Transwell assay, flow cytometry analysis and Western blot, respectively. The regulatory relationship between LINC00115 and miR-489-3p was determined by dual-luciferase reporter assays. Results LINC00115 was significantly overexpressed in CRC and its overexpression predicted poor outcome of the patients. Downregulation of LINC00115 markedly inhibited CRC cell proliferation, increased cell apoptosis, and suppressed cell migration and invasion. Moreover, downregulation of LINC00115 led to the inactivation of PI3K/AKT/mTOR signaling. Bioinformatics analysis identified miR-489-3p as a candidate target of LINC00115. Furthermore, we revealed an inverse correlation between LINC00115 and miR-489-3p in CRC tissues. miR-489-3p might directly target LINC00115 and downregulation of miR-489-3p could rescue the biological effects induced by the absence of LINC0015. Conclusion LINC00115 serves as an excellent oncogene of CRC metastasis, the deeper understanding of LINC00115/miR-489-3p axis might provide potential therapeutic targets for CRC metastasis.

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Long non-coding RNA TUG1 mediates 5-fluorouracil resistance by acting as a ceRNA of miR-197-3p in colorectal cancer

Cited by 61 publications

References 37 publications

Long Non-coding RNA LINC00115 Contributes to the Progression of Colorectal Cancer by Targeting miR-489-3p via the PI3K/AKT/mTOR Pathway

Long Non-coding RNA LINC00115 Contributes to the Progression of Colorectal Cancer by Targeting miR-489-3p via the PI3K/AKT/mTOR Pathway

<p>Inhibition of CDK1 Reverses the Resistance of 5-Fu in Colorectal Cancer</p>

Long non-coding RNA LINC00115 contributes to the progression of colorectal cancer by targeting miR-489-3p via PI3K/AKT/mTOR pathway

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