Gastric cancer (GC) is one of the most common
cancers in the world. The
cathepsin F (CTSF) gene has recently been found to participate in the progression of several types of
cancer. However, the clinical characteristics and function of CTSF in GC as well as its molecular mechanisms are not clear. Six GC cell lines and 44 paired adjacent noncancerous and GC tissue samples were used to assess CTSF expression by quantitative polymerase chain reaction (qPCR). We used lentivirus-mediated
small hairpin RNA (Lenti-
shRNA) against CTSF to knock down the expression of CTSF in GC cells. Western blot and qPCR were used to analyze the
mRNA and related
protein expression. The
biological phenotypes of gastric cells were examined by cell proliferation and apoptosis assays. Microarray-based
mRNA expression profile screening was also performed to evaluate the potential molecular pathways in which CTSF may be involved. The CTSF
mRNA level was associated with
tumor differentiation, depth of
tumor invasion, and
lymph node metastasis. Downregulation of CTSF expression efficiently inhibited apoptosis and promoted the proliferation of GC cells. Moreover, a total of 1,117 upregulated mRNAs and 1,143 downregulated mRNAs were identified as differentially expressed genes (DEGs). Further analysis identified the involvement of these mRNAs in
cancer-related pathways and various other biological processes. Nine DEGs in
cancer-related pathways and three downstream genes in the apoptosis pathway were validated by Western blot, which was mainly in agreement with the microarray data. To our knowledge, this is the first report investigating the effect of CTSF on the growth and apoptosis in GC cells and its clinical significance. The CTSF gene may function as a
tumor suppressor in GC and may be a potential therapeutic target in the treatment of GC.