Metastasis Of Non-small Lung Cancer Research Articles

PPIP5K2 Facilitates Proliferation and Metastasis of Non-Small Lung Cancer (NSCLC) through AKT Signaling Pathway

PPIP5K2 Facilitates Proliferation and Metastasis of Non-Small Lung Cancer (NSCLC) through AKT Signaling Pathway

Study on the mechanism of long non-coding RNA migration inhibitory factor antisense RNA1 in regulating proliferation, invasion and metastasis of non-small cell lung cancer

Objective To explore the molecular mechanism by which long non-coding RNA (lncRNA) migration inhibitory factor antisense RNA1 (MIF-AS1)/microRNA (miRNAM miR)-370-3p/mitogen activated protein kinase 9 (MAP3K9) molecular axis regulates proliferation, invasion and migration of non-small cell lung cancer (NSCLC). Methods Twenty cancer samples of NSCLC patients were collected from Henan Provincial People’s Hospital from May 2017 to January 2019. There were 12 males and 8 females, aged (52.37±10.34) years. Real-time quantitative reverse transcriptase-polymerase chain reaction (RT-qPCR) and Western blotting were used to detect the expression levels of MIF-AS1, miR-370-3p and MAP3K9 in cancer tissues and 9 cell lines. NSCLC A549 cells were transfected with si-MIF-AS1, si-NC, si-MIF-AS1+ anti-miR-370-3p or si-MIF-AS1+ pcDNA-MAP3K9, respectively. Methyl thiazol tetrazolium (MTT) assay and Transwell assay were used to detect the proliferation, migration and invasion of transfected cells. Western blotting was used to detect the expression of Cyclin D1, p21, p27, matrix metalloproteinase (MMP)-2, MMP-9 and MMP-14 proteins. The dual luciferase reporter gene verified the targeting regulation of MIF-AS1 on miR-370-3p and miR-370-3p on MAP3K9. Results The expression of MIF-AS1 and MAP3K9 in NSCLC tissues (2.49±0.25 and 2.24±0.22) and A549 cells (2.54±0.24 and 2.31±0.23), H1299 cells (2.11±0.21 and 2.44±0.24) and PC-9 cells (2.26±0.23 and 2.16±0.22) was significantly higher than that in adjacent tissues (1.00±0.09 and 1.02±0.09) and normal lung epithelial cells BEAS-2B (1.01±0.09 and 1.00±0.09) (t=25.078, P<0.05; F=94.367, P<0.05). The expression of miR-370-3p in NSCLC tissues (0.42±0.04), A549 cells (0.34±0.03), H1299 cells (0.53±0.05), and PC-9 cells (0.44±0.04) was significantly lower than that in adjacent tissues (1.01±0.08) and BEAS-2B cells (1.00±0.08) (t=29.500, P<0.05; F=269.552, P<0.05). Transfection with si-MIF-AS1 significantly inhibited NSCLC cell proliferation (24 h: 0.27±0.03, 48 h: 0.36±0.03, 72 h: 0.48±0.04), invasion (24.33±3.14), migration (32.46±3.34) ability (P<0.01), up-regulated p21 (0.64±0.06), p27 (0.77±0.07) protein expression (t=17.441, P<0.05; t=17.726, P<0.05) and down-regulated Cyclin D1 (0.29±0.03), MMP-2 (0.25±0.03), MMP-9 (0.34±0.03) and MMP-14 (0.29±0.03) protein expression (t=17.732, P<0.05). The dual luciferase reporter gene confirmed that MIF-AS1 was bond to miR-370-3p and miR-370-3p was bond to MAP3K9. Transfection with si-MIF-AS1+ anti-miR-370-3p or si-MIF-AS1+ pcDNA-MAP3K9 inhibited the effects of si-MIF-AS1 on proliferation, invasion and migration of NSCLC cells. Conclusion LncRNA MIF-AS1 promotes proliferation, migration and invasion of NSCLCs by regulating miR-370-3p/MAP3K9 molecular axis. Key words: Non-small cell lung cancer; Long non-coding RNA migration inhibitory factor antisense RNA1; MicroRNA-370-3p; Mitogen activated protein kinase 9; Proliferation; Migration; Invasion

Overexpression of Raf-1 kinase inhibitor protein inhibits cell invasion and migration in lung cancer cells through suppressing epithelial-mesenchymal transition

Background: Raf-1 kinase inhibitor protein (RKIP) is a small evolutionary conserved protein that was associated with the Raf-MEK-ERK pathway. However, whether RKIP would alter the invasion and metastasis of non-small cell lung cancer (NSCLC) and play the role through suppressing epithelial-mesenchymal transition (EMT) remains to be explored. Methods: A549 cells were transfected with RKIP-GV141 plasmid for overexpression of RKIP. Colony formation assay and MTT assay were performed to measure the effects of RKIP on the proliferation and cell viability assay of A549 cells. Transwell, Migration Assay and wound healing assay were performed to analyze the effects of RKIP on the invasion and metastasis of A549 cells. E-cadherin and vimentin were measured by Western blot to conform RKIP affects invasion and metastasis of NSCLC via inhibiting EMT. Results: RKIP is downregulated in NSCLC tissues compared to adjacent normal lung tissues by IHC. Decreased expression of RKIP contributes to poor prognosis in lung adenocarcinoma patients. Age and pTNM stage were independent prognostic factors for adenocarcinoma patients. Overexpression of RKIP reduces the cell viability and limits the proliferation, invasion, and migration of A549 cells in vitro . Wound healing assay showed the degressive ability of metastasis. High expression of E-cadherin and low expression of vimentin indicated that RKIP affects invasion and metastasis of NSCLC via inhibiting EMT. Conclusions: RKIP is decreased in NSCLC tissues. Overexpression of RKIP in A549 cells would decrease the cellular proliferation, viability, invasion ability, and metastasis ability probably via inhibiting EMT through upregulating E-cadherin expression and downregulating vimentin expression.

Clinical application of circRNA in non-small cell lung cancer

Lung cancer is one of the most common cancers in the world, which seriously affects people′s physical and mental health. About 85% of them are non-small cell lung cancers. In recent years, with the rapid development of low-dose computed tomography, Da Vinci robotic surgery and targeted therapy, the therapeutic effect of lung cancer has been greatly improved. However, due to the lack of early diagnosis of biomarkers, therapeutic targets and signs of prognosis, most patients have metastases when they are at the time of treatment. Lung cancer remains the leading cause of cancer-related death. CircRNA is a special endogenous non coding RNA, which is formed by the reverse splicing of the 3′ splice donor site and the 5′ splice acceptor site to form a covalent closed loop. It is highly conservative and stable. The expression level of circRNA in non-small cell lung cancer is obviously abnormal, which is closely related to the occurrence, development and metastasis of non-small cell lung cancer. It is expected to become an ideal biomarker, which is used for early diagnosis of non-small cell lung cancer, and provides new therapeutic targets and prognostic markers. Key words: Non-small-cell lung cancer; Diagnosis; Molecular targeted therapy; Prognosis; Non-coding RNA

Role of VEGF-C in metastasis of non-small cell lung cancer

Vascular endothelial growth factor-C (VEGF-C) can promote the growth of tumor thymphangiogenesis by binding with receptor VEGFR-2 and VEGFR-3. It is an important factor of tumor lymphatic metastasis. Lymphatic metastasis is the major diffusion way for non-small cell lung cancer(NSCLC).The over expression of VEGF-C is significantly correlated to metastasis and prognosis of NSCLC. This article rewiews the bionomics and the functions of VEGF-C in metastasis of NSCLC. Key words: Vascular endothelial growth factor C; Carcinoma,non-small-cell lung; Neoplasm metastasis

Relationship between MMP and non-small-cell lung carcinma

The matrix metalloproteinases (MMPs) are highly conservative families of zinc-dependent endopeptidases.MMPs are essential enzymes which are involved in the degradation of basement membrane and the extracellular matrix, and play an important role in the tumor invasion and metastasis.MMPs can be classi-fied into collagenases ,gelatinases, matrilysins, membrane type MMPs( MT-MMPs), and other undefined MMPs The MT-MMPs are membrane-tethered proteolytic enzymes and constitute the largest family of MMPs identified so far, other four types are secretory MMPs.MT-MMPs play a vital role in the progression and metastasis of non-small cell lung cancer for their location and structual specificity. Key words: Carcinoma,non-small-cell lung; Matrix metalloproteinases