To investigate the effects of SKA3 on cell proliferation and metastasis in non-small-cell lung cancer (NSCLC) and its underlying mechanism. Immunohistochemistry was employed to analyze the expression of SKA3 in NSCLC. CCK-8 assay, EdU assay, Transwell assay and flow cytometry analysis were employed to assess cell proliferation, metastatic potential and apoptosis , respectively. A lung metastasis model was used to evaluate metastasis of NSCLC cells  A luciferase reporter gene assay was conducted to verify the targeting relationship. SKA3 exhibited high expression in NSCLC tissues and cells. Overexpression of SKA3 remarkably accelerated cell proliferation and metastasis and suppressed apoptosis of NSCLC cells and promoted lung metastasis in a mouse model. repressed SKA3 expression by targeting it. inhibited the progression of NSCLC through targeting SKA3.

Download full-text PDF

Source
http://dx.doi.org/10.2217/pme-2020-0095DOI Listing

Publication Analysis

Top Keywords

cell proliferation
12
non-small-cell lung
8
lung cancer
8
proliferation metastasis
8
lung metastasis
8
nsclc cells
8
nsclc
6
metastasis
5
ska3
5
negatively regulated
4

Similar Publications

Perivascular adipose tissue: a central player in the triad of diabetes, obesity, and cardiovascular health.

Cardiovasc Diabetol

December 2024

Institute of Physiology, iCBR, Faculty of Medicine, University of Coimbra, Subunit 1, polo 3, Azinhaga de Santa Comba, Celas, 3000-548, Coimbra, Portugal.

Perivascular adipose tissue (PVAT) is a dynamic tissue that affects vascular function and cardiovascular health. The connection between PVAT, the immune system, obesity, and vascular disease is complex and plays a pivotal role in the pathogenesis of vascular diseases such as atherosclerosis, hypertension, and vascular inflammation. In cardiometabolic diseases, PVAT becomes a significant source of proflammatory adipokines, leading to increased infiltration of immune cells, in cardiometabolic diseases, PVAT becomes a significant source of proinflammatory adipokines, leading to increased infiltration of immune cells, promoting vascular smooth muscle cell proliferation and migrationpromoting vascular smooth muscle cell proliferation and migration.

View Article and Find Full Text PDF

Background: Cutaneous melanoma is one of the most invasive and lethal skin malignant tumors. Compared to primary melanoma, metastatic melanoma (MM) presents poorer treatment outcomes and a higher mortality rate. The tumor microenvironment (TME) plays a critical role in MM progression and immunotherapy resistance.

View Article and Find Full Text PDF

Insulin-like growth factor II mRNA-binding proteins (IGF2BPs), a family of RNA-binding proteins, are pivotal in regulating RNA dynamics, encompassing processes such as localization, metabolism, stability, and translation through the formation of ribonucleoprotein complexes. First identified in 1999 for their affinity to insulin-like growth factor II mRNA, IGF2BPs have been implicated in promoting tumor malignancy behaviors, including proliferation, metastasis, and the maintenance of stemness, which are associated with unfavorable outcomes in various cancers. Additionally, non-coding RNAs (ncRNAs), particularly long non-coding RNAs, circular RNAs, and microRNAs, play critical roles in cancer progression through intricate protein-RNA interactions.

View Article and Find Full Text PDF

HIF-1α mediates hypertension and vascular remodeling in sleep apnea via hippo-YAP pathway activation.

Mol Med

December 2024

Department of Otorhinolaryngology/Head and Neck, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, No.3 East Qingchun Road, Hangzhou, 310020, Zhejiang, China.

Background: Sleep apnea syndrome (SAS) is associated with hypertension and vascular remodeling. Hypoxia-inducible factor-1α (HIF-1α) and the Hippo-YAP pathway are implicated in these processes, but their specific roles remain unclear. This study investigated the HIF-1α/Hippo-YAP pathway in SAS-related hypertension.

View Article and Find Full Text PDF

TIMP-2 Promotes Wound Healing by Suppressing Matrix Metalloproteinases and Inflammatory Cytokines in Corneal Epithelial Cells.

Am J Pathol

December 2024

Schepens Eye Research Institute of Massachusetts Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, MA 02114, USA. Electronic address:

Tissue inhibitors of metalloproteinases (TIMPs) modulate extracellular matrix (ECM) remodeling for maintaining homeostasis and promoting cell migration and proliferation. Pathological conditions can alter TIMP homeostasis and aggravate disease progression. The roles of TIMPs have been studied in tissue-related disorders; however, their contributions to tissue repair during corneal injury are undefined.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!