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Kinesin superfamily protein 21B acts as an oncogene in non-small cell lung cancer
Zhi-Gang Sun1, Feng Pan2, Jing-Bo Shao3
1Department of Thoracic Surgery, Central Hospital Affiliated to Shandong First Medical University, Jinan, 250013 People's Republic of China.
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.
Insights
Kinesin family member 21B (KIF21B) is upregulated in non-small cell lung cancer (NSCLC) and promotes tumor growth and metastasis. Silencing KIF21B inhibits NSCLC progression, suggesting it is a potential therapeutic target for NSCLC.
Area of Science:
- Oncology
- Molecular Biology
- Cell Biology
Background:
- Kinesin superfamily proteins (KIFs) are microtubule-dependent motors implicated in cancer progression.
- The specific role of kinesin family member 21B (KIF21B) in non-small cell lung cancer (NSCLC) requires detailed investigation.
Purpose of the Study:
- To investigate the expression pattern of KIF21B in NSCLC.
- To elucidate the precise role of KIF21B in the growth and metastasis of NSCLC cells.
- To evaluate KIF21B as a potential therapeutic target and prognostic biomarker for NSCLC.
Main Methods:
- Immunohistochemical staining (IHC) to assess KIF21B expression in 72 NSCLC tissues.
- shRNA-mediated KIF21B knockdown in NSCLC cell lines (H1299, A549) and normal lung cells (BEAS-2B).
- Functional assays including CCK8, colony formation, Hoechst 33342/PI staining, wound-healing, and Transwell assays to evaluate proliferation, apoptosis, migration, and invasion. Western blot for apoptosis-related proteins and in vivo studies using a nude mouse model.
Main Results:
- KIF21B was significantly upregulated in NSCLC tissues and correlated with lymph node metastasis and advanced pTNM stage, predicting poor prognosis.
- KIF21B knockdown suppressed NSCLC cell proliferation, induced apoptosis (evidenced by altered Bcl-2, Bax, and active Caspase 3 expression), and reduced levels of p-Akt and Cyclin D1.
- Silencing KIF21B inhibited NSCLC cell migration and invasion, and significantly reduced tumor growth in vivo, without affecting normal lung cells.
Conclusions:
- KIF21B is overexpressed in NSCLC and functions as an oncogene promoting tumor growth and metastasis.
- KIF21B inhibition demonstrates anti-cancer effects in NSCLC models.
- KIF21B represents a promising therapeutic target and prognostic biomarker for NSCLC.
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