Browsing by Subject "KIF2A"

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    Circ_SATB2 knockdown inhibits the tumorigenesis of non-small cell lung cancer via miR-760/KIF2A axis
    (Universidad de Murcia. Departamento de Biología Celular e Histología, 2023) Zheng, Pengchao; Jiang, Jianhua; Li, Lei; Wei, Liang; Li, Jie; Jin, Ling
    Purpose. This study was aimed at exploring the function and underlying mechanism of circ_SATB2 in non-small cell lung cancer (NSCLC). Methods. The levels of circ_SATB2, microRNA-760 (miR-760) and Kinesin family member 2a (KIF2A) were determined using quantitative real-time polymerase chain reaction or western blot assay. The proliferation was detected using MTT and colony formation assays. Cell cycle and apoptosis were evaluated by flow cytometry. Transwell assay for migration and invasion and western blot for metastasis-associated proteins were conducted. Dual-luciferase reporter assay was used to analyze the interaction between miR-760 and circ_SATB2 or KIF2A. The effect of circ_SATB2 on NSCLC tumor growth in vivo was studied by xenograft mice model. Results. Circ_SATB2 was upregulated in NSCLC tissues and cells. Circ_SATB2 knockdown caused inhibitory effects on NSCLC cell proliferation and metastasis but accelerated apoptosis. Circ_SATB2 served as a sponge of miR-760 to act in the development of NSCLC. Moreover, miR-760 could target KIF2A, and KIF2A expression was positively regulated by circ_SATB2. Furthermore, KIF2A overexpression neutralized miR-760-mediated inhibition effects on NSCLC cell progression. Besides, circ_SATB2 enhanced NSCLC tumorigenesis by targeting miR760/KIF2A axis in vivo. Conclusion. Circ_SATB2 was highly expressed and participated in the progression of NSCLC through the modulation of the miR-760/KIF2A axis, suggesting that circ_SATB2 might be a potential biomarker for the diagnosis of NSCLC.
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    Hsa_circ_0088036 promotes tumorigenesis and chemotherapy resistance in hepatocellular carcinoma via the miR-140-3p/KIF2A axis
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2025) Wang, Zhong; Wang, Lei; Yin, Guoqing; Li, Heng; Zhang, Rong; Feng, Yuan; Chang, Wen; Biología Celular e Histología
    Background. Hepatocellular carcinoma (HCC) is a cancer with high morbidity and mortality. There are limited treatment options, particularly for chemotherapy-resistant HCC patients. Circular RNA hsa_circ_0088036 was associated with the development of bladder cancer and non-small cell lung cancer. However, whether it might be a potential therapeutic target for HCC remains elusive. Methods. Hsa_circ_0088036 expression was detected in HCC tumor tissues and cell lines using real-time PCR. The influences of hsa_circ_0088036 on proliferation and invasion as well as chemotherapy sensitivity in HCC cells were investigated by gain- and loss-of-function analyses. Associations among hsa_circ_0088036, miR-140-3p, and KIF2A were validated by real-time PCR, miRNA pull-down assay, dual-luciferase reporter assay, and western blot. Furthermore, a rescue experiment using KIF2A overexpression was performed to evaluate the regulatory mechanism of hsa_circ_0088036 in HCC cells. Additionally, the effect and mechanism of hsa_circ_0088036 were confirmed in a xenograft mouse model. Results. Hsa_circ_0088036 was highly expressed in HCC tissues and cells, with even higher expression in oxaliplatin-resistant cells. This expression was positively correlated with tumor size and TNM stage of the patients. Overexpression of hsa_circ_0088036 promoted the proliferation and invasion of HCC cells, while silencing mediated the opposite effects. Meanwhile, knockdown of hsa_circ_0088036 enhanced chemo-therapy sensitivity, including oxaliplatin, doxorubicin, and sorafenib, in HCC cells. Furthermore, hsa_circ_ 0088036 silencing inhibited tumor growth and increased oxaliplatin sensitivity in vivo. Mechanically, hsa_circ_0088036 functioned via the miR-140-3p/KIF2A axis with the activation of PI3K/Akt and Notch signaling pathways. Conclusions. Hsa_circ_0088036 promoted HCC tumorigenesis and chemotherapy resistance by activating the PI3K/Akt and Notch pathways through regulating miR-140-3p/KIF2A signaling. Thus, hsa_circ_0088036 may be a potential therapeutic target in chemotherapy-resistant HC