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Published on: October 27, 2014
Upregulation of KIN17 is associated with non-small cell lung cancer invasiveness
Yuzhao Zhang1, Senlin Huang1, Hongyi Gao2
1Laboratory Medicine Center, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, P.R. China.
Abstract:
Kin17 DNA and RNA binding protein (Kin17) is a highly conserved protein that participates in DNA replication, DNA repair and cell cycle progression. Recently, the tumor-promoting function of Kin17 has been demonstrated and increasingly studied. In the present study, the role of Kin17 in the invasion and metastasis of non-small cells lung cancer (NSCLC) was investigated. Elevated Kin17 mRNA and protein expression was identified in a total of 97 NSCLC and benign lung lesion tissue specimens. Kin17 overexpression was significantly correlated with high tumor grade and lymph node metastasis, indicating poor patient prognosis. Scratch and Transwell assays demonstrated that the knockdown of KIN17 inhibited the ability of NSCLC cells to migrate and invade. Furthermore, reverse transcription-quantitative polymerase chain reaction and western blot analyses confirmed that knockdown of KIN17 decreased the expression of matrix metalloproteinase 7, epidermal growth factor receptor and v-myc avian myelocytomatosis viral oncogene homolog. The results of the present study indicate that Kin17 is markedly overexpressed in NSCLC tissues compared with benign lung lesion and peritumoral tissue. The upregulation of KIN17 may serve an important role in the metastasis of NSCLC cells. These results indicate that Kin17 is a novel diagnostic and prognostic biomarker of NSCLC, in addition to being a potential therapeutic target for the treatment of patients with NSCLC.
Insights
Kin17 protein promotes non-small cell lung cancer (NSCLC) metastasis. Lowering Kin17 levels inhibits cancer cell invasion and may offer a new therapeutic target for NSCLC treatment.
Area of Science:
- Molecular Biology
- Oncology
- Cancer Research
Background:
- Kin17 DNA and RNA binding protein (Kin17) is a conserved protein involved in DNA replication, repair, and cell cycle.
- Recent studies highlight Kin17's tumor-promoting functions.
- The role of Kin17 in non-small cell lung cancer (NSCLC) metastasis requires further investigation.
Purpose of the Study:
- To investigate the role of Kin17 in the invasion and metastasis of NSCLC.
- To determine if Kin17 expression correlates with clinical parameters and patient prognosis in NSCLC.
- To explore Kin17 as a potential diagnostic and therapeutic target for NSCLC.
Main Methods:
- Analysis of Kin17 mRNA and protein expression in 97 NSCLC and benign lung tissues.
- Correlation analysis between Kin17 expression, tumor grade, and lymph node metastasis.
- In vitro assays (scratch and Transwell) to assess NSCLC cell migration and invasion after KIN17 knockdown.
- Quantitative polymerase chain reaction and Western blot to evaluate the expression of downstream targets.
Main Results:
- Kin17 mRNA and protein were significantly upregulated in NSCLC tissues compared to benign tissues.
- Elevated Kin17 expression correlated with high tumor grade and lymph node metastasis, indicating poor prognosis.
- Knockdown of KIN17 significantly inhibited NSCLC cell migration and invasion.
- Kin17 knockdown reduced the expression of matrix metalloproteinase 7, epidermal growth factor receptor, and v-myc avian myelocytomatosis viral oncogene homolog.
Conclusions:
- Kin17 is overexpressed in NSCLC and plays a crucial role in promoting tumor cell metastasis.
- Kin17 serves as a potential diagnostic and prognostic biomarker for NSCLC.
- Targeting Kin17 may represent a novel therapeutic strategy for NSCLC treatment.
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