Expression and Function of FERMT Genes in Colon Carcinoma Cells
ANTICANCER RESEARCH
Authors: Kiriyama, Kenji; Hirohashi, Yoshihiko; Torigoe, Toshihiko; Kubo, Terufumi; Tamura, Yasuaki; Kanaseki, Takayuki; Takahashi, Akari; Nakazawa, Emiri; Saka, Eri; Ragnarsson, Charlotte; Nakatsugawa, Munehide; Inoda, Satoko; Asanuma, Hiroko; Takasu, Hideo; Hasegawa, Tadashi; Yasoshima, Takahiro; Hirata, Koichi; Sato, Noriyuki
Abstract
Invasion into the matrix is one of hallmarks of malignant diseases and is the first step for tumor metastasis. Thus, analysis of the molecular mechanisms of invasion is essential to overcome tumor cell invasion. In the present study, we screened for colon carcinoma-specific genes using a cDNA microarray database of colon carcinoma tissues and normal colon tissues, and we found that fermitin family member-1 (FERMT1) is overexpressed in colon carcinoma cells. FRRMT1, FERMT2 and FERMT3 expression was investigated in colon carcinoma cells. Reverse transcription polymerase chain reaction (RT-PCR) analysis revealed that only FERMT1 had cancer cell-specific expression. Protein expression of FERMT1 was confirmed by western blotting and immunohistochemical staining. To address the molecular functions of FERMT genes in colon carcinoma cells, we established FERMT1-, FERMT2- and FERMT3-overexpressing colon carcinoma cells. FERMT1-overexpressing cells exhibited greater invasive ability than did FERMT2- and FERMT3-overexpressing cells. On the other hand, FERMT1-, FERMT2- and FERMT3-overexpressing cells exhibited enhancement of cell growth. Taken together, the results of this study indicate that FERMT1 is expressed specifically in colon carcinoma cells, and has roles in matrix invasion and cell growth. These findings indicate that FERMT1 is a potential molecular target for cancer therapy.
Prognostic Implications of Novel Gene Signatures in Gastric Cancer Microenvironment
MEDICAL SCIENCE MONITOR
Authors: Sun, Mengyu; Qiu, Jieping; Zhai, Huazheng; Wang, Yaoqun; Ma, Panpan; Li, Mengying; Chen, Bo
Abstract
Background: Increasing studies have shown the important clinical role of immune and stromal cells in gastric cancer microenvironment. Based on information of immune and stromal cells in The Cancer Genome Atlas, this study aimed to construct a prognostic risk assessment model for gastric cancer. Material/Methods: Based on the immune/structural scores, differentially expressed genes (DEGs) were filtered and analyzed. Afterwards, DEGs associated with prognosis were screened and the risk assessment model was constructed in the training set. Moreover, the validity of the model was verified both in the testing set and the overall sample. Results: In this study, patients were divided into high-score and low-score groups based on immune/stromal score, and 919 DEGs were identified. By applying least absolute shrinkage and selection operator (LASSO) and Cox analysis, 10 mRNAs were selected to form a prognostic risk assessment model, risk score=(0.294*SLC17A9) + (-0.477*FERMT3) + (0.866*NRP1) + (0.350*MMRN1) + (0.381*RNASE1) + (0.189*TRIB3) + (0.230*PGAP3) + (0.087*MAGEA3) + (0.182*TACR2) + (0.368*CYP51A1). In the training set, the low-risk group divided by the model was found to have better overall survival, and the prediction efficiency of the model was demonstrated to be good. Multivariate Cox analysis indicated that the model could work as a prognostic factor independently. Similar results were shown in the testing group and overall patients cohort group. Finally, the risk assessment model and other clinical variables were integrated to construct a nomogram. Conclusions: In general, this study constructs a prognostic risk assessment model for gastric cancer, which could improve the prognosis stratification of patients combined with other clinical indicators.