Pyrroline-5-Carboxylate Reductase 1 Accelerates the Migration and Invasion of Nonsmall Cell Lung Cancer In Vitro

2019 ◽  
Vol 34 (6) ◽  
pp. 380-387 ◽  
Author(s):  
Senhua Sang ◽  
Cuicui Zhang ◽  
Jianwei Shan
2011 ◽  
Vol 5 (1) ◽  
pp. 69-76 ◽  
Author(s):  
Jian Fan ◽  
Li Zhang ◽  
Qi long Wang ◽  
Hui Lin

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.


2021 ◽  
Vol 16 (9) ◽  
pp. 1934578X2110332
Author(s):  
Pham T. Hong Minh ◽  
Tran T. Hoai Van ◽  
Tran Q. Toan ◽  
Le M. Bui ◽  
Nguyen H. Thuan Anh ◽  
...  

Annual mortality of 8.2 million could be attributable to cancer globally, posing a serious health issue; particularly, the high number of nonsmall cell lung cancer (NSCLC) diagnosed cases in recent years highlight the need for development in anticancer agents. In NSCLC, a number of specific inhibitors of phosphatidylinositol-3-kinase (PI3K), Protein kinase B (AKT), and mammalian target of rapamycin are currently under development; however, the early evidence has yielded disappointing results. Ent-kaurane diterpenoid compounds from Cronton tonkinensis have been investigated for several bioactivities such as antibacterial, cytotoxic activity, and so on;; however, lung cancer is not yet studied. In this study, we conducted a molecular docking study of 7 ent-kaurane diterpenoids from C tonkinensis against PI3K targeted anticancer therapies; furthermore, their cytotoxicity effects against A549 lung cancer cells were also evaluated. Obtained results indicated that compounds 7, 6, 2, and 1 exhibited significant inhibitory results in comparison to the reference drug oxaliplatin which suggests further in vitro assay for drug development.


2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Jie-Yao Li ◽  
Xiu-Fang Duan ◽  
Li-Ping Wang ◽  
Yu-Jie Xu ◽  
Lan Huang ◽  
...  

Regulatory T (Treg) cells are potent suppressors that maintain immune homeostasis. Accumulation of Treg can inhibit effective immune responses in cancer patients, leading to tumor development and progression. Despite direct cytotoxicity, several chemotherapeutic drugs have been reported to deplete Treg cells for better prognosis for cancer patients. Treg cells are a heterogenous population with at least three different subsets, nonsuppressive, resting, and activated Treg cells. However, the characteristics of Treg cell subsets in lung cancer patients and how chemotherapy affects Treg cells remain elusive. In this study, we first analyzed Treg cell subsets in peripheral blood samples from 40 nonsmall cell lung cancer (NSCLC) patients and 20 healthy donors. Treg cells, specifically activated Treg cell subset, significantly increased in patients with NSCLC. Compared to nonsuppressive Treg cells, activated Treg cells expressed higher level of CD39 and predominantly produced inhibitory cytokines.In vitroassay showed that docetaxel reduced all three subsets of Treg cells. More importantly, we found docetaxel-based chemotherapy significantly decreased all three Treg subsets after 4 cycles of treatment in 17 NSCLC patients. Taken together, this study revealed dynamic changes of various Treg cell subsets in NSCLC patients before and after chemotherapy, providing activated Treg cells as a potential target for chemotherapy.


2006 ◽  
Vol 81 (2) ◽  
pp. 440-447 ◽  
Author(s):  
Thomas A. d’Amato ◽  
Rodney J. Landreneau ◽  
Robert J. McKenna ◽  
Ricardo S. Santos ◽  
Ricardo J. Parker

Author(s):  
Ziyi Wang ◽  
Xinyu Zhang ◽  
Xuedong Zhang ◽  
Xuedong Jiang

Long intergenic nonprotein coding RNA 1703 (LINC01703) has diagnostic significancein lung adenocarcinoma. However, its specific roles in non-small-cell lung cancer(NSCLC) and downstream mechanisms have not been investigated. In the current study,we characterized the role of LINC01703 in NSCLC malignancy and elucidated itsdetailed mechanism of action. LINC01703 expression was measured by qRT-PCR. Theregulatory effects of LINC01703 on the malignancy of NSCLC cells were assessed bymultiple functional experiments. The targeted interaction was confirmed by RNAimmunoprecipitation and luciferase reporter assays. Herein, overexpression ofLINC01703 in NSCLC was indicated in the TCGA database and further proven in ourcohort. Functional studies revealed that knocking down LINC01703 repressed cellproliferation, colony formation, migration and invasion in vitro, which wasaccompanied by the induction of apoptosis. The tumor growth of LINC01703-silencedcells was also inhibited in vivo. Mechanistic analyses revealed that LINC01703functioned as a competing endogenous RNA for microRNA-605-3p (miR-605-3p) inNSCLC cells, which thereby upregulated the miR-605-3p target metastasis associatedwith colon cancer 1 (MACC1). Rescue experiments highlighted that the regulatoryactions of LINC01703 ablation on NSCLC cells were abolished in response to miR-605-3p downregulation or MACC1 overexpression. In conclusion, LINC01703enhanced the aggressiveness of NSCLC cells by altering miR-605-3p/MACC1. Ourwork suggests the therapeutic potential of LINC01703/miR-605-3p/MACC1 in NSCLC.


2021 ◽  
pp. 1-9
Author(s):  
Li-Na Pan ◽  
Yun-Fang Ma ◽  
Jia-An Hu ◽  
Zhi-Hong Xu

Circular RNA (circRNA) has been shown to participate in various tumors, including lung cancer. In the present study, we explored the expression and functional relevance of hsa_circ_0003288 in human non-small cell lung cancer (NSCLC). We verified that hsa_circ_0003288 expression was upregulated in lung cancer tissues and cell lines. Overexpression of hsa_circ_0003288 dramatically promoted lung cancer cell proliferation, colony formation, inhibited apoptosis, and increased cell migration and invasion in vitro. Xenograft experiments showed that hsa_circ_0003288 overexpression accelerated tumor growth in vivo. Mechanistically, hsa_circ_0003288 negatively regulated miR-145 to exert the oncogenic role in lung cancer. Overexpression of miR-145 decreased cell proliferation, induced apoptosis, and suppressed migration and invasion in lung cancer. Additionally, miR-145 co-transfection abolished the oncogenic role of hsa_circ_0003288. Collectively, these findings identified a novel regulatory role of hsa_circ_0003288/miR-145 axis in the progression of NSCLC.


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