Current studies have demonstrated that SLC38A1 proteins play a causal role in neoplastic cell transformation. The twofold aim of this study was to provide insight into whether a variance in the expression of SLC38A1 exists between human colorectal cancer and healthy human tissues and to determine how silencing or overexpressing the SLC38A1 gene could affect the proliferation, viability and migration of colorectal cancer cells. Immunohistochemical staining was used to analyze the expression of SLC38A1 in colorectal cancer tissues and adjacent normal mucosa in 77 patients who underwent surgical resection. The expression of SLC38A1 in colorectal cancer tissues and cell lines was detected using RT-PCR and Western blotting. Two colorectal cancer cell lines SW480 and HCT116 were used to examine whether silencing SLC38A1 with siRNA and overexpressing SLC38A1 with shRNA could affect cell viability and migration. As a result, the SLC38A1 protein was very low or undetectable in the normal colon mucosa. In contrast, strong staining of SLC38A1 protein was found in the cytoplasm in 79.2% colorectal cancer samples. More pronounced SLC38A1 expression in colorectal cancer tissues was significantly associated with tumor node metastasis (TNM) stage. Inhibition of SLC38A1 reduced tumour growth and suppressed proliferation and migration of SW480 cells. In contrast, overexpression of SLC38A1 had the opposite effects on HCT116 cells. SLC38A1 is overexpressed in colorectal cancer, which suggests that it is associated with tumour progression. These results encourage the exploration of SLC38A1 as a target for intervention in colorectal cancer.
The Grainyhead-like 3 (GRHL3) is involved in epidermal barrier formation, neural tube closure and wound repair. Previous studies have suggested that GRHL3 has been linked to many different types of cancers. However, to date, its effects on human colorectal cancer (CRC) has not been clarified yet. Our microarray analysis has indicated predominant GRHL3 expression in CRC. The purpose of this study was to investigate the expression and significance of GRHL3 in CRC tumorigenesis using CRC tissues and paired paracancerous tissues, as well as using distinct CRC cell lines (HT29 and DLD1). We observed increased GRHL3 expression at both mRNA and protein levels in CRC tissues and CRC cell lines using quantitative real-time polymerase chain reaction (qRT-PCR) and Western blotting. Moreover, silencing GRHL3 with siRNA could suppress CRC cell proliferation, viability and migration in vitro. We also found that knockdown of GRHL3 could promote cell cycle arrest at G/G phase in HT29 cells and DLD1 cells, and induce cell apoptosis in HT29 cells. Together, our study revealed the down-regulation of GRHL3 in vitro could inhibit CRC cell activity and trigger cell cycle arrest at G/G phase and apoptosis.
MicroRNA-454 (miR-454), is involved in the progression of various types of cancers. The present study aimed to evaluate the effect of miR-454 on the progression of gastric cancer. SGC-7901 cells overexpressing or silencing miR454 were constructed via transfection and the survival rate of the cells was determined. The relationship between miR-454 and cylindromatosis (CYLD) was explored and the influence of miR-454 on oxaliplatin resistance was investigated in SGC-7901 cells. It was determined that overexpression of miR-454 increased the number of colonies and reduced apoptosis rate of SGC-7901 cells. The CYLD gene was identified as a direct target of miR-454. miR-454 overexpression downregulated the expression of CYLD, leading to an increase in SGC-7901 cell proliferation. Finally, miR-454 was also demonstrated to induce resistance to oxaliplatin in gastric cancer cells. In conclusion, the present in vitro findings suggested that miR-454 might be a novel therapeutic target for gastric cancer.
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