Knockdown SNHG20 Suppresses Nonsmall Cell Lung Cancer Development by Repressing Proliferation, Migration and Invasion, and Inducing Apoptosis by Regulating miR-2467-3p/E2F3

2020 ◽  
Author(s):  
Hang Chen ◽  
Xin Tan ◽  
Yi Ding
Keyword(s):  
Lung Cancer ◽  
Cell Lung Cancer ◽  
Nonsmall Cell Lung Cancer ◽  
Cancer Development ◽  
Migration And Invasion

scholarly journals Serial Cancer Development Three Times in a Patient with Fanconi Anemia

2021 ◽  
pp. 1168-1174
Author(s):  
Katsuya Yanagisawa ◽  
Toshimichi Horiuchi ◽  
Akemi Matsuo ◽  
Hiroshi Kuraishi ◽  
Hidetoshi Satomi ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Solid Tumors ◽  
Fanconi Anemia ◽  
Cell Lung Cancer ◽  
Bone Marrow Failure ◽  
Nonsmall Cell Lung Cancer ◽  
Cancer Development ◽  
Hematopoietic Stem ◽  
Anal Squamous Cell Carcinoma ◽  
Increased Risk

Fanconi anemia (FA) is characterized clinically by bone marrow failure, congenital malformations, sensitivity to DNA cross-linking agents, and increased risk of malignancy. Hematological cancer is the best-described malignancy in patients with FA, but the susceptibility to the development of solid tumors is also well documented, especially after hematopoietic stem cell transplantation (HSCT). With regard to the development of solid tumors in patients with FA, head and neck, esophageal, and anal squamous cell carcinoma are well known, but reports of lung cancer are extremely rare. Here, we describe an FA patient with a history of HSCT that developed 3 serial cancers – oral, esophageal, and nonsmall cell lung cancer – over a period of 6 years. The third lesion was nonsmall cell lung cancer and its location corresponded closely to the field of irradiation treatment for prior esophageal cancer. The occurrence of lung cancer in patients with FA is uncommon, but FA patients should be screened regularly and serially. Our case also indicated the importance of the irradiated field as a location for subsequent cancer development.

scholarly journals Long noncoding RNA CYTOR sponges miR-195 to modulate proliferation, migration, invasion and radiosensitivity in nonsmall cell lung cancer cells

2018 ◽  
Vol 38 (6) ◽  
Author(s):  
Jun Zhang ◽  
Wenqi Li
Keyword(s):  
Lung Cancer ◽  
Cell Lung Cancer ◽  
Noncoding Rna ◽  
Nonsmall Cell Lung Cancer ◽  
Underlying Mechanism ◽  
Migration And Invasion ◽  
Functional Roles ◽  
Promising Therapeutic Target ◽  
Microrna Sponge

Nonsmall cell lung cancer (NSCLC) is one of the most frequent malignancies worldwide. Long noncoding RNAs (LncRNAs) play critical roles in cancer initiation and progression. Previous studies have demonstrated that overexpression of cytoskeleton regulator RNA (CYTOR) predicates poor prognosis and promotes tumor progression. However, the functional roles and underlying mechanism of CYTOR in NSCLC remain unknown. In the present study, we found that CYTOR promoted cell proliferation, migration and invasion ability, and induced radioresistance in NSCLC cells. Mechanistically, CYTOR could directly interact with miR-195 and increase its targets. Thus, CYTOR played an oncogenic role in NSCLC progression through sponging miR-195. Together, our study elucidates the role of CYTOR as a microRNA sponge in NSCLC, and CYTOR may be used as a promising therapeutic target for NSCLC treatment.

scholarly journals Chemokine receptor 9 high-expression involved in the migration and invasion of the non-small-cell lung cancer cells

2011 ◽  
Vol 5 (1) ◽  
pp. 69-76 ◽  
Author(s):  
Jian Fan ◽  
Li Zhang ◽  
Qi long Wang ◽  
Hui Lin
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Cell Lung Cancer ◽  
Chemokine Receptor ◽  
Nsclc Patient ◽  
Nonsmall Cell Lung Cancer ◽  
Migration And Invasion ◽  
Cancer Tissue ◽  
Squamous Lung Cancer

Abstract Background: Metastasis is responsible for most cancer-related death, and the metastatic spread of neoplastic cells may be related to the ability of migration and invasion. Chemokine receptor 9 (CCR9) plays an important role in cutaneous melanoma and prostate cancer cells migration and invasion. Objective: Investigate the specific role of the chemokine-ligand (CCR9-CCL25) axis in the development of nonsmall cell lung cancer (NSCLC) metastasis. Methods: Semi-quantitative reverse transcriptase-PCR, western-blot, flow cytometry, migration, and invasion assays were used to examine the function of CCR9 in the NSCLC cells. Results: CCR9 was highly expressed in NSCLC patient cancer tissue. In addition, in vitro migration and invasion studies on human bronchial epithelial cells of the BEAS-2B and human squamous lung cancer cell lines NCI-H157 showed that migration in response to the CCL25 was inhibited by CCR9 antibody. Conclusion: CCR9 might play an important role in the migration and invasion of the NSCLC cells.

The Key microRNAs Regulated the Development of Non-small Cell Lung Cancer by Targeting TGF-β-induced epithelial–mesenchymal Transition

2019 ◽  
Vol 22 (4) ◽  
pp. 238-244 ◽  
Author(s):  
Gang Chen ◽  
Bo Ye
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lines ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Nsclc Cell ◽  
Normal Lung ◽  
Migration And Invasion ◽  
Small Cell Lung ◽  
Mesenchymal Transition

Purpose: Epithelial-to-Mesenchymal Transition (EMT) was reported to play a key role in the development of Non-Small Cell Lung Cancer (NSCLC). The process of EMT is regulated by the changes of miRNAs expression. However, it is still unknown which miRNA changed the most in the process of canceration and whether these changes played a role in tumor development. Methods: A total of 36 SCLC patients treated in our hospital between 11th, 2015 and 10th, 2017 were enrolled. The samples of cancer tissues and paracancer tissues of patients were collected and analyzed. Then, the miRNAs in normal lung cells and NSCLC cells were also analyzed. In the presence of TGF-β, we transfected the miRNA mimics or inhibitor into NSCLC cells to investigate the role of the significantly altered miRNAs in cell migration and invasion and in the process of EMT. Results: MiR-330-3p was significantly up-regulated in NSCLC cell lines and tissues and miRNA- 205 was significantly down-regulated in NSCLC cell lines and NSCLC tissues. Transfected miRNA-205 mimics or miRMA-330-3p inhibitor inhibited the migration and invasion of NCIH1975 cell and restrained TGF-β-induced EMT in NSCLC cells. Conclusion: miRNA-330-3p and miRNA-205 changed the most in the process of canceration in NSCLC. Furthermore, miR-330-3p promoted cell invasion and metastasis in NSCLC probably by promoting EMT and miR-205 could restrain NSCLC likely by suppressing EMT.

scholarly journals Silibinin Regulates Tumor Progression and Tumorsphere Formation by Suppressing PD-L1 Expression in Non-Small Cell Lung Cancer (NSCLC) Cells

Cells ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1632
Author(s):  
Alexis Rugamba ◽  
Dong Young Kang ◽  
Nipin Sp ◽  
Eun Seong Jo ◽  
Jin-Moo Lee ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Growth Factor ◽  
Small Cell Lung Cancer ◽  
Anticancer Activity ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Migration And Invasion ◽  
Dependent Manner ◽  
Molecular Signaling ◽  
Small Cell Lung

Recently, natural compounds have been used globally for cancer treatment studies. Silibinin is a natural compound extracted from Silybum marianum (milk thistle), which has been suggested as an anticancer drug through various studies. Studies on its activity in various cancers are undergoing. This study demonstrated the molecular signaling behind the anticancer activity of silibinin in non-small cell lung cancer (NSCLC). Quantitative real-time polymerase chain reaction and Western blotting analysis were performed for molecular signaling analysis. Wound healing assay, invasion assay, and in vitro angiogenesis were performed for the anticancer activity of silibinin. The results indicated that silibinin inhibited A549, H292, and H460 cell proliferation in a concentration-dependent manner, as confirmed by the induction of G0/G1 cell cycle arrest and apoptosis and the inhibition of tumor angiogenesis, migration, and invasion. This study also assessed the role of silibinin in suppressing tumorsphere formation using the tumorsphere formation assay. By binding to the epidermal growth factor receptor (EGFR), silibinin downregulated phosphorylated EGFR expression, which then inhibited its downstream targets, the JAK2/STAT5 and PI3K/AKT pathways, and thereby reduced matrix metalloproteinase, PD-L1, and vascular endothelial growth factor expression. Binding analysis demonstrated that STAT5 binds to the PD-L1 promoter region in the nucleus and silibinin inhibited the STAT5/PD-L1 complex. Altogether, silibinin could be considered as a candidate for tumor immunotherapy and cancer stem cell-targeted therapy.

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