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HELLS Knockdown Inhibits the Malignant Progression of Lung Adenocarcinoma Via Blocking Akt/CREB Pathway by Downregulating KIF11.
Yang, Gang; Fu, Jinsong; Wang, Jiawei; Ding, Mei.
Afiliación
  • Yang G; Department of Thoracic Surgery, Tongling Municipal Hospital, 2999 Changjiang West Road, Tongguanshan District, Tongling, 244000, Anhui, China. yanggang890324@163.com.
  • Fu J; Department of Thoracic Surgery, Tongling Municipal Hospital, 2999 Changjiang West Road, Tongguanshan District, Tongling, 244000, Anhui, China.
  • Wang J; Department of Thoracic Surgery, Tongling Municipal Hospital, 2999 Changjiang West Road, Tongguanshan District, Tongling, 244000, Anhui, China.
  • Ding M; PRINCIPLE Biotechnology Co, Hefei, 230000, Anhui, China.
Mol Biotechnol ; 2024 Mar 13.
Article en En | MEDLINE | ID: mdl-38478260
ABSTRACT
Lung adenocarcinoma (LUAD) is a malignant tumor with the characteristics of progressive advancement and high mortality rate worldwide. We aimed to explore the role and mechanism of helicase Lymphoid-Specific (HELLS) in LUAD. Bioinformatics databases were applied to predict HELLS and kinesin family member (KIF)11 expression in LUAD tissues. The expressions of HELLS and KIF11 before and after HELLS knockdown were detected by RT-qPCR and western blot. After HELLS was knocked down, the proliferative, migratory, and invasive capabilities of A549 cells were evaluated. Cell apoptotic level was assessed using TUNEL. Western blot was employed to evaluate the expressions of Akt/CREB pathway-related proteins. The interaction between HELLS and KIF11 was analyzed using bioinformatics databases, and testified by Co-IP assay. Results revealed that HELLS and KIF11 expressions were significantly upregulated in LUAD cells and tissues. High HELLS and KIF11 expression was correlated with the poor prognosis of patients with LUAD. Additionally, HELLS knockdown suppressed the capabilities of LUAD cells to proliferate, migrate, and invade whereas promoted the cell apoptotic level. Moreover, HELLS could interact with KIF11 and had positive correlation with KIF11. Furthermore, KIF11 overexpression partially counteracted the impacts of HELLS knockdown on cell proliferative, migratory, invasive capabilities, and apoptotic level in LUAD cells. Besides, Akt/CREB pathway was blocked by HELLS silencing, which was restored by KIF11 overexpression. Collectively, HELLS knockdown blocked Akt/CREB pathway by downregulating KIF11 expression, thereby inhibiting LUAD cell proliferation, invasion, migration, and promoting apoptosis.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: Mol Biotechnol Asunto de la revista: BIOLOGIA MOLECULAR / BIOTECNOLOGIA Año: 2024 Tipo del documento: Article País de afiliación: China Pais de publicación: Suiza
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: Mol Biotechnol Asunto de la revista: BIOLOGIA MOLECULAR / BIOTECNOLOGIA Año: 2024 Tipo del documento: Article País de afiliación: China Pais de publicación: Suiza