Background: LINC00958, a newly identified lncRNA, has been reported to be closely linked to tumorigenesis in multiple cancers. However, its specific role in non-small cell lung cancer (NSCLC) remains unclear.
Methods: The expression of LINC00958 was determined by RT-qPCR analysis. Cell proliferation and migration were evaluated by CCK-8 and transwell assays, respectively. Xenograft tumor models were established to examine the effect of LINC00958 on tumor growth in vivo. Luciferase reporter assays were performed to determine the interaction between LINC00958 and miR-204-3p and the interaction between miR-204-3p and KIF2A.
Results: We found that LINC00958 was up-regulated in NSCLC tissues and cell lines. Down-regulation of LINC00958 inhibited cell proliferation and migration in vitro and suppressed tumor growth in vivo. Mechanically, we revealed that LINC00958 influenced NSCLC progression partly by sponging miR-204-3p and regulating KIF2A expression.
Conclusions: Our study provided new insights into the role of LINC00958 as a promising prognostic biomarker and a therapeutic target for NSCLC.

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Posted 18 Feb, 2020
On 28 Jun, 2021
Received 27 Jun, 2021
Received 27 Jun, 2021
Received 18 May, 2021
On 06 May, 2021
On 29 Apr, 2021
Invitations sent on 28 Feb, 2020
On 23 Feb, 2020
On 22 Feb, 2020
On 17 Feb, 2020
On 15 Feb, 2020
Posted 18 Feb, 2020
On 28 Jun, 2021
Received 27 Jun, 2021
Received 27 Jun, 2021
Received 18 May, 2021
On 06 May, 2021
On 29 Apr, 2021
Invitations sent on 28 Feb, 2020
On 23 Feb, 2020
On 22 Feb, 2020
On 17 Feb, 2020
On 15 Feb, 2020
Background: LINC00958, a newly identified lncRNA, has been reported to be closely linked to tumorigenesis in multiple cancers. However, its specific role in non-small cell lung cancer (NSCLC) remains unclear.
Methods: The expression of LINC00958 was determined by RT-qPCR analysis. Cell proliferation and migration were evaluated by CCK-8 and transwell assays, respectively. Xenograft tumor models were established to examine the effect of LINC00958 on tumor growth in vivo. Luciferase reporter assays were performed to determine the interaction between LINC00958 and miR-204-3p and the interaction between miR-204-3p and KIF2A.
Results: We found that LINC00958 was up-regulated in NSCLC tissues and cell lines. Down-regulation of LINC00958 inhibited cell proliferation and migration in vitro and suppressed tumor growth in vivo. Mechanically, we revealed that LINC00958 influenced NSCLC progression partly by sponging miR-204-3p and regulating KIF2A expression.
Conclusions: Our study provided new insights into the role of LINC00958 as a promising prognostic biomarker and a therapeutic target for NSCLC.

Figure 1

Figure 2

Figure 3

Figure 4

Figure 5

Figure 6

Figure 7

Figure 8
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