Effects of miR-21 Mediating Nerve Cell Adhesion Molecule (NCAM) and Glial Cell-Line Derived Neurotrophic Factor (GDNF) Signals on the Proliferation and Apoptosis of Lung Cancer Cells

2021 ◽  
Vol 11 (9) ◽  
pp. 1769-1773
Author(s):  
Dongliang Li ◽  
Chaoqun Dong ◽  
Zejun Fu ◽  
Yongming Song
Keyword(s):  
Lung Cancer ◽  
Cell Proliferation ◽  
Cell Adhesion ◽  
Cancer Cells ◽  
Cell Line ◽  
Adhesion Molecule ◽  
Neurotrophic Factor ◽  
Cell Apoptosis ◽  
Cell Adhesion Molecule ◽  
Proliferation And Apoptosis

Our study assessed the effect of miR-21 mediating Nerve Cell Adhesion Molecule (NCAM) and Glial Cell-line Derived Neurotrophic Factor (GDNF) on the proliferation and apoptosis of lung cancer cells. Lung cancer cell-line H460 cells were grouped as Lung cancer group (LC group) (normal cultivation); Mimic group (SI group) which was transfected with 120 nmol/L miR-21 mimics and liposomes; Inhibitor group (IN group) (transfection of miR-21 inhibitor and liposomes) followed by analysis of cell apoptosis by Hoechst 33258 staining, GDNF level by immunohistochemistry, miR-21 level by qRT-PCR, cell proliferation by CCK-8 and NCAM level by western blot. miR-21 content was significantly increased in SI group, indicating a successful transfection. The nucleus shrinkage rate in IN group and LC group was higher than SI group (P <0.05) and IN group had highest number of apoptotic cells, lowest cell proliferation and NCAM level among three groups (P <0.05). SI group showed significantly higher positive GDNF staining than IN and LC group (both P <0.05). miR-21 promotes H460 cell proliferation and inhibits cell apoptosis by upregulating NCAM and GDNF.

Role of L1 cell adhesion molecule in gastric carcinoma.

2011 ◽  
Vol 29 (4_suppl) ◽  
pp. 56-56
Author(s):  
T. Ito ◽  
Y. Kodera ◽  
C. Tanaka ◽  
N. Ohashi ◽  
G. Nakayama ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Adhesion ◽  
Mrna Expression ◽  
Cancer Cells ◽  
Cell Line ◽  
Adhesion Molecule ◽  
Cell Adhesion Molecule ◽  
Parental Cell ◽  
Parental Cell Line ◽  
L1 Cell Adhesion Molecule

56 Background: L1 cell adhesion molecule (L1) is a 200-220 kDa transmembrane glycoprotein of the immunoglobulin super family initially identified in neural cells. L1 was detected in ovarian cancer in a stage-dependent manner, was found exclusively in the invasion front of colorectal cancer, and has been considered a stem cell marker in glioma. The authors have shown that mRNA expression of L1 was a significant prognostic factor in gastric cancer (Kodera et al. Gastrointestinal Cancer Symposium 2009, abst 37). Its role in gastric cancer was further investigated. Methods: Expression of L1 was observed by immunostaining in 72 surgically resected pT4A-stage gastric cancer specimens. The association of L1 with peritoneal seeding and prognosis was elucidated. mRNA expression of L1-expressing gastric cancer cell line, KATO3, was suppressed using siRNA (KATO3 L1-). Microarray was used to indentify molecules that differ in expression between KATO3 L1- and the parental cell line. Results: L1 was scarcely stained in non-cancerous epithelial cells and intestinal metaplastic cells. L1 was detected mainly in the cell surface membrane of cancer cells in 15 of 72 specimens, more often in the intestinal type cancer. No correlation was found between L1 expression and detection of cancer cells in the peritoneal washes or development of peritoneal carcinomatosis. Nevertheless, the prognosis of L1-positive cancer was significantly inferior (p = 0.024). Prognosis was particularly poor among 6 cases where L1 was expressed in cancer cells at the invasive front (median survival time 149 days). Of 40,000 genes evaluated in the microarray, mRNA expression of 50 genes were amplified by > 4-fold whereas the expression of 20 genes were attenuated to less than 1/4. Of these, expression of DYRK1A that induces apoptosis in conjunction with p53 was markedly suppressed to less than 1/8. Suppression of DYRK1A in the KATO3 L1- in comparison with the parental cell line was confirmed by RT-PCR. Conclusions: L1 affects prognosis of gastric cancer, particularly when it is expressed in cancer cells at the invasion front. Its role in the biology of gastric cancer has began to be elucidated. No significant financial relationships to disclose.

scholarly journals Pivotal role of epithelial cell adhesion molecule in the survival of lung cancer cells

2011 ◽  
Vol 102 (8) ◽  
pp. 1493-1500 ◽  
Author(s):  
Tetsunari Hase ◽  
Mitsuo Sato ◽  
Kenya Yoshida ◽  
Luc Girard ◽  
Yoshihiro Takeyama ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Adhesion ◽  
Epithelial Cell ◽  
Cancer Cells ◽  
Adhesion Molecule ◽  
Cell Adhesion Molecule ◽  
Pivotal Role ◽  
Lung Cancer Cells ◽  
Epithelial Cell Adhesion Molecule

scholarly journals The role of epithelial cell adhesion molecule N-glycosylation on apoptosis in breast cancer cells

Tumor Biology ◽  
2017 ◽  
Vol 39 (3) ◽  
pp. 101042831769597 ◽  
Author(s):  
Dandan Zhang ◽  
Xue Liu ◽  
Jiujiao Gao ◽  
Yan Sun ◽  
Tingjiao Liu ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Cell Adhesion ◽  
Epithelial Cell ◽  
Cancer Cells ◽  
Adhesion Molecule ◽  
Breast Cancer Cells ◽  
Cell Adhesion Molecule ◽  
Mitogen Activated Protein Kinase ◽  
Epithelial Cell Adhesion Molecule

Glycosylation of cell surface proteins plays an important role in the regulation of apoptosis. It has been demonstrated that knockdown of epithelial cell adhesion molecule promoted apoptosis, inhibited cell proliferation, and caused cell-cycle arrest. In this study, we investigated whether and how N-glycosylation of epithelial cell adhesion molecule influenced the apoptosis in breast cancer cells. We applied the N-glycosylation mutation epithelial cell adhesion molecule plasmid to express deglycosylation of epithelial cell adhesion molecule and then to study its function. Our results showed that deglycosylation of epithelial cell adhesion molecule promoted apoptosis and inhibited cell proliferation. Deglycosylation of epithelial cell adhesion molecule enhanced the cytotoxic effect of 5-fluorouracil, promoting apoptosis by downregulating the expression of the anti-apoptotic protein Bcl-2 and upregulating the expression of the pro-apoptotic proteins Bax and Caspase 3 via the extracellular-signal-regulated kinase 1/2 and c-Jun N-terminal kinase mitogen-activated protein kinase signaling pathways in MCF-7 and MDA-MB-231 cells. These findings are important for a better understanding of epithelial cell adhesion molecule apoptosis regulation and suggest epithelial cell adhesion molecule as a potential target for the treatment of breast cancer.

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