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Primary research
Kinesin superfamily protein 21B acts as an oncogene in non-small cell lung cancer
Nan Zhang
jinan central hospital
Corresponding Author
ORCiD: https://orcid.org/0000-0002-6744-2810
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Background: Kinesin superfamily proteins (KIFs) serve as microtubule-dependent molecular motors, and are involved in the progression of many malignant tumors. In this study, we aimed to investigate the expression pattern and precise role of kinesin family member 21B (KIF21B) in non-small cell lung cancer (NSCLC).
Methods: KIF21B expression in 72 cases of NSCLC tissues was measured by immunohistochemical staining (IHC). We used shRNA-KIF21B interference to silence KIF21B in NSCLC H1299 and A549 cells and normal lung epithelial bronchus BEAS-2B cells. The biological roles of KIF21B in the growth and metastasis abilities of NSCLC cells were measured by Cell Counting Kit-8 (CCK8), colony formation and Hoechst 33342/PI, wound-healing, and Transwell assays, respectively. Expression of apoptosis-related proteins was determined using western blot. The effect of KIF21B on tumor growth in vivo was examined using nude mice model.
Results: KIF21B was up-regulated in NSCLC tissues, and correlated with pathological lymph node and pTNM stage, its high expression was predicted a poor prognosis of patients with NSCLC. Silencing of KIF21B mediated by lentivirus-delivered shRNA significantly inhibited the proliferation ability of H1299 and A549 cells. KIF21B knockdown increased apoptosis in H1299 and A549 cells, down-regulated the expression of Bcl-2 and up-regulated the expression of Bax and active Caspase 3. Moreover, KIF21B knockdown decreased the level of phosphorylated form of Akt (p-Akt) and Cyclin D1 expression in H1299 and A549 cells. In addition, silencing of KIF21B impeded the migration and invasion of H1299 and A549 cells. Further, silencing of KIF 21B dramatically inhibited xenograft growth in BALB/c nude mice. However, silencing of KIF21B did not affect the proliferation, migration and invasion of BEAS-2B cells.
Conclusions: These results reveal that KIF21B is up-regulated in NSCLC and acts as an oncogene in the growth and metastasis of NSCLC, which may function as a potential therapeutic target and a prognostic biomarker for NSCLC.
Keywords
non-small cell lung cancer, KIF21B, proliferation, oncogene
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Received 02 Jun, 2020
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Reviewer #1 agreed
On 29 May, 2020
Reviewer #2 agreed
On 29 May, 2020
Review #1 received
Received 29 May, 2020
Editor assigned
On 28 May, 2020
Submission checks complete
On 27 May, 2020
Editor invited
On 27 May, 2020
No comments provided
Review #3 received
Received 27 Apr, 2020
Editorial decision: Major revision
On 27 Apr, 2020
Review #2 received
Received 26 Apr, 2020
Review #1 received
Received 26 Apr, 2020
Reviewer #3 agreed
On 16 Apr, 2020
Editor assigned
On 13 Apr, 2020
Reviewers invited
Invitations sent on 13 Apr, 2020
Reviewer #1 agreed
On 13 Apr, 2020
Reviewer #2 agreed
On 13 Apr, 2020
Editor invited
On 12 Apr, 2020
Submission checks complete
On 05 Apr, 2020
First submitted
On 03 Apr, 2020
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Subject Areas
Oncology
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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
Kinesin superfamily protein 21B acts as an oncogene in non-small cell lung cancer
Nan Zhang
jinan central hospital
Corresponding Author
ORCiD: https://orcid.org/0000-0002-6744-2810
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 2
Posted 04 Jun, 2020
No community comments so far
Review #2 received
Received 02 Jun, 2020
Reviewers invited
Invitations sent on 29 May, 2020
Reviewer #1 agreed
On 29 May, 2020
Reviewer #2 agreed
On 29 May, 2020
Review #1 received
Received 29 May, 2020
Editor assigned
On 28 May, 2020
Submission checks complete
On 27 May, 2020
Editor invited
On 27 May, 2020
No comments provided
Review #3 received
Received 27 Apr, 2020
Editorial decision: Major revision
On 27 Apr, 2020
Review #2 received
Received 26 Apr, 2020
Review #1 received
Received 26 Apr, 2020
Reviewer #3 agreed
On 16 Apr, 2020
Editor assigned
On 13 Apr, 2020
Reviewers invited
Invitations sent on 13 Apr, 2020
Reviewer #1 agreed
On 13 Apr, 2020
Reviewer #2 agreed
On 13 Apr, 2020
Editor invited
On 12 Apr, 2020
Submission checks complete
On 05 Apr, 2020
First submitted
On 03 Apr, 2020
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Subject Areas
Oncology
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Background: Kinesin superfamily proteins (KIFs) serve as microtubule-dependent molecular motors, and are involved in the progression of many malignant tumors. In this study, we aimed to investigate the expression pattern and precise role of kinesin family member 21B (KIF21B) in non-small cell lung cancer (NSCLC).
Methods: KIF21B expression in 72 cases of NSCLC tissues was measured by immunohistochemical staining (IHC). We used shRNA-KIF21B interference to silence KIF21B in NSCLC H1299 and A549 cells and normal lung epithelial bronchus BEAS-2B cells. The biological roles of KIF21B in the growth and metastasis abilities of NSCLC cells were measured by Cell Counting Kit-8 (CCK8), colony formation and Hoechst 33342/PI, wound-healing, and Transwell assays, respectively. Expression of apoptosis-related proteins was determined using western blot. The effect of KIF21B on tumor growth in vivo was examined using nude mice model.
Results: KIF21B was up-regulated in NSCLC tissues, and correlated with pathological lymph node and pTNM stage, its high expression was predicted a poor prognosis of patients with NSCLC. Silencing of KIF21B mediated by lentivirus-delivered shRNA significantly inhibited the proliferation ability of H1299 and A549 cells. KIF21B knockdown increased apoptosis in H1299 and A549 cells, down-regulated the expression of Bcl-2 and up-regulated the expression of Bax and active Caspase 3. Moreover, KIF21B knockdown decreased the level of phosphorylated form of Akt (p-Akt) and Cyclin D1 expression in H1299 and A549 cells. In addition, silencing of KIF21B impeded the migration and invasion of H1299 and A549 cells. Further, silencing of KIF 21B dramatically inhibited xenograft growth in BALB/c nude mice. However, silencing of KIF21B did not affect the proliferation, migration and invasion of BEAS-2B cells.
Conclusions: These results reveal that KIF21B is up-regulated in NSCLC and acts as an oncogene in the growth and metastasis of NSCLC, which may function as a potential therapeutic target and a prognostic biomarker for NSCLC.
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
Figure 6