scholarly journals Overexpression of CXCR7 Accelerates Tumor Growth and Metastasis of Lung Cancer Cells

2020 ◽  
Author(s):  
Liu Huan ◽  
Cheng Qian ◽  
Xu Dong sheng ◽  
Wang Wen ◽  
Fang Zheng ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Migration ◽  
Human Lung ◽  
Lung Tumor ◽  
Xenograft Model ◽  
Cell Polarization ◽  
Human Lung Cancer ◽  
Migration And Invasion ◽  
Mouse Xenograft ◽  
Mouse Xenograft Model

Abstract Background: Under physiological conditions, CXCL12 modulates cell proliferation, survival, angiogenesis, and migration mainly through CXCR4. Interestingly, the newly discovered receptor CXCR7 for CXCL12 is highly expressed in many tumor cells as well as tumor-associated blood vessels, although the level of CXCR7 in normal cells is low. Recently, many studies have suggested that CXCR7 promotes cell growth and metastasis in more than 20 human malignancies, among which lung cancer is the leading cause of cancer-associated deaths worldwide. Thus, the mechanism of CXCR7 in the progression of lung cancer is urgently needed.Methods: First, we explored CXCR4 and CXCR7 expression in human lung cancer specimens and cell lines by immunohistochemistry, western blot and flow cytometry. Then, we chose the human lung adenocarcinoma cell line A549 that stably overexpressed CXCR7 through the way of lentivirus-mediated transduction. Next, “wound healing” assay and transwell assay were applied to compare the cell migration and invasion ability, and stripe assay was used to evaluate the cell polarization. Last, our team established a mouse xenograft model of human lung cancer and monitored tumor proliferation and metastasis by firefly luciferase bioluminescence imaging in SCID/Beige mice. Results: In clinical lung cancer samples, CXCR7 expression was almost not detected in normal tissue but upregulated in lung tumor tissue, whereas, CXCR4 was highly expressed in both normal and tumor tissues. Furthermore, overexpression of CXCR7 enhanced A549 cell migration and polarization in vitro. Besides, mouse xenograft model of human lung cancer showed that CXCR7 promoted primary lung tumor’s growth and metastasis to the second organ, such as liver or bone marrow in SCID/Beige mice in vivo.Conclusions: This study describes the multiple functions of CXCR7 in lung cancer. Thus, these results suggest that CXCR7 may be a malignancy marker and may provide a novel target for anticancer therapy.

scholarly journals Overexpression of CXCR7 accelerates tumor growth and metastasis of lung cancer cells

2020 ◽  
Vol 21 (1) ◽  
Author(s):  
Huan Liu ◽  
Qian Cheng ◽  
Dong-sheng Xu ◽  
Wen Wang ◽  
Zheng Fang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Migration ◽  
Human Lung ◽  
Lung Tumor ◽  
Xenograft Model ◽  
Cell Polarization ◽  
Human Lung Cancer ◽  
Migration And Invasion ◽  
Mouse Xenograft ◽  
Mouse Xenograft Model

Abstract Background Under physiological conditions, CXCL12 modulates cell proliferation, survival, angiogenesis, and migration mainly through CXCR4. Interestingly, the newly discovered receptor CXCR7 for CXCL12 is highly expressed in many tumor cells as well as tumor-associated blood vessels, although the level of CXCR7 in normal cells is low. Recently, many studies have suggested that CXCR7 promotes cell growth and metastasis in more than 20 human malignancies, among which lung cancer is the leading cause of cancer-associated deaths worldwide. Thus, the mechanism of CXCR7 in the progression of lung cancer is urgently needed. Methods First, we explored CXCR4 and CXCR7 expression in human lung cancer specimens and cell lines by immunohistochemistry, western blot and flow cytometry. Then, we chose the human lung adenocarcinoma cell line A549 that stably overexpressed CXCR7 through the way of lentivirus-mediated transduction. Next, “wound healing” assay and transwell assay were applied to compare the cell migration and invasion ability, and stripe assay was used to evaluate the cell polarization. Last, our team established a mouse xenograft model of human lung cancer and monitored tumor proliferation and metastasis by firefly luciferase bioluminescence imaging in SCID/Beige mice. Results In clinical lung cancer samples, CXCR7 expression was almost not detected in normal tissue but upregulated in lung tumor tissue, whereas, CXCR4 was highly expressed in both normal and tumor tissues. Furthermore, overexpression of CXCR7 enhanced A549 cell migration and polarization in vitro. Besides, mouse xenograft model of human lung cancer showed that CXCR7 promoted primary lung tumor’s growth and metastasis to the second organ, such as liver or bone marrow in SCID/Beige mice in vivo. Conclusions This study describes the multiple functions of CXCR7 in lung cancer. Thus, these results suggest that CXCR7 may be a malignancy marker and may provide a novel target for anticancer therapy.

scholarly journals Overexpression of CXCR7 Enhances Metastasis on Lung Cancer Cell

2020 ◽  
Author(s):  
Liu Huan ◽  
Cheng Qian ◽  
Xu Dong sheng ◽  
Wang Wen ◽  
Fang Zheng ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Migration ◽  
Human Lung ◽  
Lung Tumor ◽  
Xenograft Model ◽  
Cell Polarization ◽  
Human Lung Cancer ◽  
Migration And Invasion ◽  
Mouse Xenograft ◽  
Mouse Xenograft Model

Abstract Background Under physiological conditions, CXCL12 modulates cell proliferation, survival, angiogenesis, and migration mainly through CXCR4. Interestingly, the newly discovered receptor CXCR7 for CXCL12 is highly expressed in many tumor cells as well as tumor-associated blood vessels, although the level of CXCR7 in normal cells is low. Recently, many studies have suggested that CXCR7 promotes cell growth and metastasis in more than 20 human malignancies, among which lung cancer is the leading cause of cancer-associated deaths worldwide. Thus, the mechanism of CXCR7 in the progression of lung cancer is urgently needed. Methods First, we explored CXCR4 and CXCR7 expression in human lung cancer specimens and cell lines by immunohistochemistry, western blot and flow cytometry. Then, we chose the human lung adenocarcinoma cell line A549 that stably overexpressed CXCR7 through the way of lentivirus-mediated transduction. Next, “wound healing” assay and transwell assay were applied to compare the cell migration and invasion ability, and stripe assay was used to evaluate the cell polarization. Last, our team established a mouse xenograft model of human lung cancer and monitored tumor proliferation and metastasis by firefly luciferase bioluminescence imaging in SCID/Beige mice. Results In clinical lung cancer samples, CXCR7 were highly expressed in lung tumor tissue compared with normal tissue, and, CXCR4 highly expressed in both normal and tumor tissues. Furthermore, overexpression of CXCR7 enhanced A549 cell migration and polarization in vitro. Besides, mouse xenograft model of human lung cancer showed that CXCR7 promoted primary lung tumor’s growth and metastasis to the second organ, such as liver or bone marrow in SCID/Beige mice in vivo. Conclusions This study describes the multiple functions of CXCR7 in lung cancer. Thus, these results suggest that CXCR7 may be a malignancy marker and may provide a novel target for anticancer therapy.

scholarly journals A HLA-A2-restricted CTL epitope induces anti-tumor effects against human lung cancer in mouse xenograft model

Oncotarget ◽  
2015 ◽  
Vol 7 (1) ◽  
pp. 671-683 ◽  
Author(s):  
Yuh-Pyng Sher ◽  
Su-I Lin ◽  
I-Hua Chen ◽  
Hsin-Yu Liu ◽  
Chen-Yuan Lin ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Human Lung ◽  
Xenograft Model ◽  
Human Lung Cancer ◽  
Mouse Xenograft ◽  
Ctl Epitope ◽  
Mouse Xenograft Model

Bufalin inhibits gefitinib resistant NCI-H460 human lung cancer cell migration and invasion in vitro

2016 ◽  
Vol 194 ◽  
pp. 1043-1050 ◽  
Author(s):  
An-Cheng Huang ◽  
Mei-Due Yang ◽  
Yung-Ting Hsiao ◽  
Tzu-Shun Lin ◽  
Yi-Shih Ma ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Migration ◽  
Cancer Cell ◽  
Human Lung ◽  
Human Lung Cancer ◽  
Migration And Invasion ◽  
Cancer Cell Migration ◽  
Lung Cancer Cell ◽  
Human Lung Cancer Cell

scholarly journals Cantharidin Impairs Cell Migration and Invasion of Human Lung Cancer NCI-H460 Cells via UPA and MAPK Signaling Pathways

2016 ◽  
Vol 36 (11) ◽  
pp. 5989-5998 ◽  
Author(s):  
TE-CHUN HSIA ◽  
CHIEN-CHIH YU ◽  
YUNG-TING HSIAO ◽  
SHIN-HWAR WU ◽  
DA-TIAN BAU ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Migration ◽  
Signaling Pathways ◽  
Human Lung ◽  
Mapk Signaling ◽  
Human Lung Cancer ◽  
Migration And Invasion ◽  
Cell Migration And Invasion ◽  
H460 Cells ◽  
Mapk Signaling Pathways

Deguelin Impairs Cell Adhesion, Migration and Invasion of Human Lung Cancer Cells through the NF-κB Signaling Pathways

2018 ◽  
Vol 46 (01) ◽  
pp. 209-229 ◽  
Author(s):  
Yung-Ting Hsiao ◽  
Ming-Jen Fan ◽  
An-Cheng Huang ◽  
Jin-Cherng Lien ◽  
Jen-Jyh Lin ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Wound Healing ◽  
Cell Migration ◽  
Cell Adhesion ◽  
Cancer Cells ◽  
Human Lung ◽  
Human Lung Cancer ◽  
Migration And Invasion ◽  
Confocal Laser ◽  
Human Lung Cancer Cells

Deguelin, a rotenoid, is isolated from a natural plant species, and has biological activities including antitumor function. In the present study, we investigated the effect of deguelin on the cell adhesion, migration and invasion of NCI-H292 human lung cancer cells in vitro. Cell viability was analyzed by using flow cytometer. Cell adhesion was determined by using the cell-matrix adhesion assay. Wound healing assay was used to examine cell migration. Cell migration and invasion were investigated using a Boyden chamber assay. The protein expression was measured by Western blotting and confocal laser microscopy. The electrophoretic mobility shift assay was used to measure NF-[Formula: see text]B p65 binding to DNA.We selected the concentrations of deguelin at 0, 0.5, 1.0, 1.5, 2.0 and 2.5[Formula: see text][Formula: see text]M and we found that those concentrations of deguelin did not induce significant cytotoxic effects on NCI-H292 cells. Thus, we selected those concentrations of deguelin for metastasis assay. We found that deguelin inhibited cell adhesion, migration and invasion in dose-dependent manners that was assayed by wound healing and transwell methods, respectively. Deguelin decreased the expression of MMP-2/-9, SOS 1, Rho A, p-AKT (Thr308), p-ERK1/2, p-p38, p-JNK, NF-[Formula: see text]B (p65) and uPA in NCI-H292 cells. Deguelin suppressed the expression of PI3K, SOS 1, NF-[Formula: see text]B (p65), but did not significantly affect PKC and Ras in the nuclei of NCI-H292 cells that were confirmed by confocal laser microscopy. We suggest that deguelin may be used as a novel anticancer metastasis of lung cancer in the future.

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