Galectin­1 binds GRP78 to promote the proliferation and metastasis of gastric cancer.

The present study aimed to investigate the potential molecular mechanisms by which galectin­1 (Gal­1) and glucose­regulated protein 78 (GRP78) influence the development of malignant gastric cancer (GC). Immunohistochemistry and western blotting were used to map the expression and location of the Gal­1 gene in the 80 paraffin­embedded GC samples, 16 fresh samples and surrounding tissues. Gal­1 was overexpressed and knocked down using lentiviral vectors in the human GC cell lines HGC­27 and AGS. Through the use of the Cell Counting Kit­8 assay, clone formation assay, wound healing assay, invasion assay and tumor xenograft, the possible biological roles of Gal­1 were further evaluated. The downstream interacting proteins were predicted by the BioGRID database, and GRP78 was chosen for further investigation. Immunofluorescence labeling and Co­IP were used to confirm the connection. The statistical tests utilized were the two­tailed paired Student's t­test, χ2 test, Kaplan­Meier and Cox regression analysis, and Spearman's rank correlation coefficients. In GC, Gal­1 is extensively expressed and has the potential to interact with GRP78. Poor prognosis is linked to high levels of GRP78 and Gal­1 expression in patients with GC. According to the functional study, Gal­1 knockdown prevented cells from thriving and pushed Gal­1 expression, which aided in the proliferation, migration and invasion of GC. Gal­1 overexpression additionally aided the development of subcutaneous xenograft tumors. The mechanistic investigation proved that GRP78 and Gal­1 interacted, accelerating the course of GC. Gal­1 silencing had an inhibitory effect on the proliferation of HGC­27 cells that was removed by ectopic GRP78 expression, whereas the stimulating effects of Gal­1 overexpression in AGS cells were inhibited by GRP78 knockdown. In conclusion, Gal­1 interacts with GRP78 to facilitate the advancement of GC. The Gal­1/GRP78 axis is supported by the functional data of the present study as a possible GC treatment target.

Morphological study of chronic prostatitis-chronic pelvic pain syndrome (CP/CPPS) normal modeling dose of T2 peptide in mice.

OBJECTIVES: However, the pathogenesis and etiology of CP/CPPS are still poorly understood. Therefore, there is a need for further research through the Image J software to develop models capable of imitating the pathogenesis and etiology of CP/CPPS with different doses of the pathogenesis and the etiology of CP/CPPS is still poorly understood. The aim was to determine the area of the prostatic interstitium, the localization of the inflammation, and the impact of different doses on the group model. MATERIALS AND METHODS: A total of 30 male ICR mice were randomly grouped into 5 (n = 6): 45 µg group = 6, 60  µg group = 6, 90  µg group = 6, 120  µg group = 6, 120  µg group = 6, control group = 6. With the exception of the control group, all the groups were immunized by injecting 0.2 mL of T2 peptide emulsion and immune adjuvant CFA to induce non-bacterial chronic prostatitis on days 0 and 14 of the mice and finally executed on day 28. All injections were administered subcutaneously. HE staining was used to evaluate changes in prostate pathology. Image J was used to calculate the area of the prostate interstitium, which represents the degree of prostate edema. To compare statistical differences between groups, the ANOVA test was used. RESULTS: From the perspective of pathological scoring, the 60 µg, 90  µg, and 120  µg groups had the highest scores using Image J to treat inflammatory cells. In addition, in the prostate interstitium area treated, it was found that the 90  µg group attained the largest prostate interstitial area as well as the highest degree of swelling. CONCLUSIONS: From the results, Image J software is an effective tool in the calculating the surface of the prostatic interstitium and the specific localization of the inflammation.