scholarly journals Silencing of LncRNA AFAP1-AS1 Inhibits Cell Proliferation in Oral Squamous Cancer by Suppressing CCNA2

2021 ◽  
Vol Volume 13 ◽  
pp. 7897-7908
Author(s):  
Tao Li ◽  
Duanqin Liu ◽  
Chenglong Li ◽  
Lu Ru ◽  
Xuixia Wang
Keyword(s):  
Cell Proliferation ◽  
Squamous Cancer

miR-338-5p inhibits cell proliferation, colony formation, migration and cisplatin resistance in esophageal squamous cancer cells by targeting FERMT2

2018 ◽  
Vol 40 (7) ◽  
pp. 883-892 ◽  
Author(s):  
Wen-Chun Lin ◽  
Li-Han Chen ◽  
Yao-Chin Hsieh ◽  
Pei-Wen Yang ◽  
Liang-Chuan Lai ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Esophageal Cancer ◽  
Colony Formation ◽  
Target Genes ◽  
Cisplatin Resistance ◽  
Treatment Strategies ◽  
Major Type ◽  
Male Population ◽  
Resistance Pathway ◽  
Squamous Cancer

AbstractEsophageal cancer is one of the leading causes of cancer death in the male population of Eastern Asia. In addition, esophageal squamous cell carcinoma (ESCC) is the major type of esophageal cancer among the world. Owing to the poor overall 5-year survival rate, novel effective treatment strategies are needed. MicroRNAs are important gene regulators that are dysregulated in many cancer types. In our previous study, we applied next-generation sequencing to demonstrate that miR-338-5p was downregulated in the tumor tissue of patients with versus without recurrence. In this study, we further studied the roles of miR-338-5p in ESCC. The expression of endogenous miR-338-5p was at lower levels in ESCC cells compared with normal cells. Functional assays showed that miR-338-5p reduced cell proliferation, colony formation, migration and cisplatin resistance in an ESCC cell line, CE-81T. Potential target genes of miR-338-5p were identified by microarray and prediction tools, and 31 genes were selected. Among these, Fermitin family homolog 2 (FERMT2) plays an oncogenic role in ESCC, so it was chosen for further study. Luciferase assays showed the direct binding between miR-338-5p and the 3′ untranslated region of FERMT2. Silencing of FERMT2 inhibited cell proliferation, colony formation, migration and cisplatin resistance. Pathway analysis revealed that the integrin-linked protein kinase signaling pathway, in which FERMT2 participates, was significantly affected by a miR-338-5p mimic. Our results suggest that miR-338-5p may play an antioncogenic role in ESCC via repressing FERMT2.

miR-26a and miR-26b inhibit esophageal squamous cancer cell proliferation through suppression of c-MYC pathway

Gene ◽  
2017 ◽  
Vol 625 ◽  
pp. 1-9 ◽  
Author(s):  
Juan Li ◽  
Yue Liang ◽  
Hao Lv ◽  
Hui Meng ◽  
Gang Xiong ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cancer Cell ◽  
Cancer Cell Proliferation ◽  
Squamous Cancer ◽  
Esophageal Squamous Cancer

Neuropilin-1 contributes to esophageal squamous cancer progression via promoting P65-dependent cell proliferation

Oncogene ◽  
2017 ◽  
Vol 37 (7) ◽  
pp. 935-943 ◽  
Author(s):  
F Shi ◽  
L Shang ◽  
L-Y Yang ◽  
Y-Y Jiang ◽  
X-M Wang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cancer Progression ◽  
Neuropilin 1 ◽  
Squamous Cancer ◽  
Dependent Cell ◽  
Esophageal Squamous Cancer

miR-203 inhibits cell proliferation and promotes cisplatin induced cell death in tongue squamous cancer

2016 ◽  
Vol 473 (2) ◽  
pp. 382-387 ◽  
Author(s):  
Jiong Lin ◽  
Yao Lin ◽  
Li Fan ◽  
Wei Kuang ◽  
Liwei Zheng ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Death ◽  
Squamous Cancer

Cell proliferation and differentiation in squamous cancer

1989 ◽  
Vol 15 (1) ◽  
pp. 19-23 ◽  
Author(s):  
S. Dische ◽  
M.I. Saunders ◽  
M.H. Bennett ◽  
G.D. Wilson ◽  
N.J. McNally
Keyword(s):  
Cell Proliferation ◽  
Cell Proliferation And Differentiation ◽  
Proliferation And Differentiation ◽  
Squamous Cancer

Fibroblasts During Hypertrophic Scar Formation and Resolution

1973 ◽  
Vol 31 ◽  
pp. 428-429
Author(s):  
C. W. Kischer
Keyword(s):  
Electron Microscopy ◽  
Scanning Electron Microscopy ◽  
Cell Proliferation ◽  
Fine Structure ◽  
Metabolic Activity ◽  
Hypertrophic Scar ◽  
Normal Skin ◽  
Ground Substance ◽  
Hypertrophic Scars ◽  
Scanning Electron

The morphology of the fibroblasts changes markedly as the healing period from burn wounds progresses, through development of the hypertrophic scar, to resolution of the scar by a self-limiting process of maturation or therapeutic resolution. In addition, hypertrophic scars contain an increased cell proliferation largely made up of fibroblasts. This tremendous population of fibroblasts seems congruous with the abundance of collagen and ground substance. The fine structure of these cells should reflect some aspects of the metabolic activity necessary for production of the scar, and might presage the stage of maturation.A comparison of the fine structure of the fibroblasts from normal skin, different scar types, and granulation tissue has been made by transmission (TEM) and scanning electron microscopy (SEM).

The Effect of Androgen Depletion and Replacement on the Epithelium of the Seminal Vesicle of the Aging Rat

1975 ◽  
Vol 33 ◽  
pp. 590-591
Author(s):  
Venita F. Allison
Keyword(s):  
Cell Proliferation ◽  
Seminal Vesicle ◽  
Male Rats ◽  
Target Cells ◽  
Cell Regeneration ◽  
Secretory Function ◽  
Electron Microscopic ◽  
Aging Rat ◽  
Microscopic Studies ◽  
Androgen Depletion

In 1930, Moore, Hughes and Gallager reported that after castration seminal vesicle epithelial cell atrophy occurred and that cell regeneration could be achieved with daily injections of testis extract. Electron microscopic studies have confirmed those observations and have shown that testosterone injections restore the epithelium of the seminal vesicle in adult castrated male rats. Studies concerned with the metabolism of androgens point out that dihydrotestosterone stimulates cell proliferation and that other metabolites of testosterone probably influence secretory function in certain target cells.Although the influence of androgens on adult seminal vesicle epithelial cytology is well documented, little is known of the effect of androgen depletion and replacement on those cells in aging animals. The present study is concerned with the effect of castration and testosterone injection on the epithelium of the seminal vesicle of aging rats.

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