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LINC00958 Promotes the Proliferation of TSCC Via miR-211-5p/CENPK Axis and Activating the JAK/STAT3 Signaling Pathway
Shuguan Liu
Department of Oral Surgery, Stomatological Hospital, Southern Medical University, 366 South Jiang Nan Road, haizhu, guangzhou, guangdong 510280, P.R. China.
Corresponding Author
ORCiD: https://orcid.org/0000-0003-0066-1020
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This work is licensed under a CC BY 4.0 License. Read Full License
Background：Tongue squamous cell carcinoma (TSCC) is one of the most common oral tumors. Recently, long intergenic noncoding RNA 00958 (LINC00958) has been identified as an oncogenic gene in human cancers. Nevertheless, the role of LINC00958 and its downstream mechanisms in TSCC is still unknown. The expression levels of LINC00958 in human TSCC tissues and adjacent normal tissues were determined.
Methods：The effect of LINC00958 on TSCC cells proliferation and growth were assessed by CCK-8, colony formation, 5-Ethynyl-2’-deoxyuridline (EdU) assay, and flow cytometry assays in vitro and tumor xenograft model in vivo. Bioinformatics analysis was used to predict the target of LINC00958 in TSCC, which was verified by RNA immunoprecipitation and luciferase reporter assays.
Results：LINC00958 was increased in TSCC tissues, and patients with high LINC00958 expression had a shorter overall survival. LINC00958 knockdown significantly decreased the growth rate of TSCC cells both in vitro and in vivo. In mechanism, LINC00958 acted as a ceRNA by competitively sponging miR-211-5p. In addition, we identified CENPK as a direct target gene of miR-211-5p, which was higher in TSCC tissues than that in adjacent normal tissues. Up-regulated miR-211-5p or down-regulated CENPK could abolish LINC00958-induced proliferation promotion in TSCC cells. Furthermore, The overexpression of CENPK promoted the expression of oncogenic cell cycle regulators and activated the JAK/STAT3 signaling.
Conclusions：Our findings suggest that LINC00958 is a potential prognostic biomarker in TSCC.
Keywords
TSCC, LINC00958, miR-211-5p, CENPK, proliferation
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This is a list of supplementary files associated with this preprint. Click to download.
- TableS2.docx
Table S2. Sequences of PCR primers used in this study.
- TableS1.docx
Table S1. Correlation of clinicopathological characteristics and gene( protein )expression in the patients.
- FigureS5.jpg
Figure S5. TCGA analysis revealed that cell cycle-related biological functions were enriched in response to high CENPK expression.
- FigureS4.jpg
Figure S4. CENPK is upregulated in TSCC. (A)The expression of CENPK were analyzed in TSCC and normal epithelial tissues by TCGA. (B) The expression of CENPK were detected in frozen TSCC (n=24) and normal epithelial tissues (n=24) by RT-qPCR.
- FigureS3.jpg
Figure S3. miR-211-5p is upregulated in TSCC and negative correlated with LINC00958 expression. (A) The expression of miR-211-5p were analyzed in TSCC and normal epithelial tissues by TCGA. (B) The expression of miR-211-5p were detected in TSCC (n=24) and normal epithelial tissues (n=24) by RT-qPCR. (C) Correlation between LINC00958 and miR-211-5p expression based on the TCGA analysis.
- FigureS2.jpg
Figure S2. The effect of LINC00958 on the migratory and invasive abilities of TSCC cells.(A and B) Representative images of Transwell migration assays of n SCC-9 and CAL-27 cells. (B) Representative images of the Wound healing assay in SCC-9 and CAL-27 cells.
- FigureS1.jpg
Figure S1. Kaplan-Meier analysis of the correlation between LINC00958 expression and overall survival in different tumors.
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This preprint is under consideration at Cancer Cell International. A preprint is a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
Learn more about In Review
Primary research
LINC00958 Promotes the Proliferation of TSCC Via miR-211-5p/CENPK Axis and Activating the JAK/STAT3 Signaling Pathway
Shuguan Liu
Department of Oral Surgery, Stomatological Hospital, Southern Medical University, 366 South Jiang Nan Road, haizhu, guangzhou, guangdong 510280, P.R. China.
Corresponding Author
ORCiD: https://orcid.org/0000-0003-0066-1020
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
Peer Review Timeline
CURRENT STATUS: Under Review
Version (no preprint)
Posted 28 Dec, 2020
Editorial decision: Minor revision
On 28 Dec, 2020
Reviewer #5 agreed
On 22 Dec, 2020
Review #1 received
Received 22 Dec, 2020
Review #5 received
Received 22 Dec, 2020
Review #3 received
Received 21 Dec, 2020
Reviewer #4 agreed
On 21 Dec, 2020
Review #4 received
Received 21 Dec, 2020
Review #2 received
Received 21 Dec, 2020
Reviewer #2 agreed
On 20 Dec, 2020
Reviewer #3 agreed
On 20 Dec, 2020
Reviewers invited
Invitations sent on 20 Dec, 2020
Reviewer #1 agreed
On 20 Dec, 2020
Editor assigned
On 20 Dec, 2020
Submission checks complete
On 20 Dec, 2020
Editor invited
On 20 Dec, 2020
This version was not preprinted
Version 1
Posted 22 Sep, 2020
No community comments so far
Editorial decision: Major revision
On 22 Oct, 2020
Review #6 received
Received 20 Oct, 2020
Review #5 received
Received 12 Oct, 2020
Review #3 received
Received 08 Oct, 2020
Review #4 received
Received 06 Oct, 2020
Reviewer #6 agreed
On 29 Sep, 2020
Reviewer #5 agreed
On 28 Sep, 2020
Review #2 received
Received 27 Sep, 2020
Reviewer #4 agreed
On 26 Sep, 2020
Reviewer #3 agreed
On 23 Sep, 2020
Reviewer #2 agreed
On 19 Sep, 2020
Review #1 received
Received 19 Sep, 2020
Reviewer #1 agreed
On 18 Sep, 2020
Reviewers invited
Invitations sent on 17 Sep, 2020
Editor assigned
On 16 Sep, 2020
First submitted
On 15 Sep, 2020
Submission checks complete
On 15 Sep, 2020
Editor invited
On 15 Sep, 2020
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Subject Areas
Cancer Biology
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Background：Tongue squamous cell carcinoma (TSCC) is one of the most common oral tumors. Recently, long intergenic noncoding RNA 00958 (LINC00958) has been identified as an oncogenic gene in human cancers. Nevertheless, the role of LINC00958 and its downstream mechanisms in TSCC is still unknown. The expression levels of LINC00958 in human TSCC tissues and adjacent normal tissues were determined.
Methods：The effect of LINC00958 on TSCC cells proliferation and growth were assessed by CCK-8, colony formation, 5-Ethynyl-2’-deoxyuridline (EdU) assay, and flow cytometry assays in vitro and tumor xenograft model in vivo. Bioinformatics analysis was used to predict the target of LINC00958 in TSCC, which was verified by RNA immunoprecipitation and luciferase reporter assays.
Results：LINC00958 was increased in TSCC tissues, and patients with high LINC00958 expression had a shorter overall survival. LINC00958 knockdown significantly decreased the growth rate of TSCC cells both in vitro and in vivo. In mechanism, LINC00958 acted as a ceRNA by competitively sponging miR-211-5p. In addition, we identified CENPK as a direct target gene of miR-211-5p, which was higher in TSCC tissues than that in adjacent normal tissues. Up-regulated miR-211-5p or down-regulated CENPK could abolish LINC00958-induced proliferation promotion in TSCC cells. Furthermore, The overexpression of CENPK promoted the expression of oncogenic cell cycle regulators and activated the JAK/STAT3 signaling.
Conclusions：Our findings suggest that LINC00958 is a potential prognostic biomarker in TSCC.
Figure 1
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Figure 3
Figure 4
Figure 5
Figure 6
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