PCMT1 Is a Potential Prognostic Biomarker and Is Correlated with Immune Infiltrates in Breast Cancer.

Background: Protein-L-isoaspartate (D-aspartate) O-methyltransferase (PCMT1) is involved in the occurrence and development of a variety of malignant tumors. However, the prognostic value of PCMT1 in breast cancer remains unclear. Methods: Based on the Cancer Genome Atlas database, we assessed the correlation between the expression of PCMT1 and prognosis, immune invasion, and tumor mutation burden in a variety of cancers. The expression level, mutation, immune correlation, and coexpression of PCMT1 in breast cancer were studied using the following databases: UALCAN database, Human Protein Atlas database, cBioPortal database, TIMER database, and LinkedOmics database. Kaplan-Meier Plotter was used for survival analysis. Receiver operating characteristic (ROC) curves and nomograms were drawn using the R software package. P < 0.05 was considered statistically significant. Results: Pancancer analysis showed that PCMT1 is highly expressed in a variety of cancers and is significantly related to the prognosis of a variety of cancers. PCMT1 is significantly related to the tumor mutation burden of a variety of cancers. PCMT1 is significantly high in breast cancer, and it is significantly related to the abundance of immune infiltration. Survival analysis revealed that high PCMT1 expression is significantly associated with shorter overall survival (OS), relapse-free survival (RFS), and postprogression survival (PPS) in breast cancer patients. ROC curves and nomograms verify the effectiveness of PCMT1 as a prognostic biomarker for breast cancer. Conclusions: PCMT1 can be used as a potential prognostic biomarker of breast cancer, and it is significantly related to the abundance of breast cancer immune infiltration.

BAG family proteins contributes to autophagy-mediated multidrug resistance of tumor.

Multidrug resistance (MDR) is a significant cause of tumor treatment failure. Accumulating evidence suggests that autophagy plays a significant role in the development of MDR. Autophagy is a conserved mechanism that maintains tumor homeostasis by removing damaged mitochondria. However, the specific regulatory mechanism is unclear. Here, we summarize recent studies on the role of autophagy in the development of MDR and the initiation of mitophagy by Bcl-2-associated athanogene (BAG) family proteins. Additionally, this mini-review emphasizes the regulatory role of BAG family proteins, which maintain mitochondrial homeostasis by regulating the PINK1/Parkin pathway. Elucidation of the regulatory mechanisms of mitophagy may foster the development of clinical therapeutic strategies for MDR tumors.

Effect of low-intensity focused ultrasound on endothelin-1, nitrogen monoxide and oxytocin receptor in the uterine tissues of Sprague-Dawley rats following abortion.

The aim of the present study was to investigate the effect of low-intensity focused ultrasound on endothelin-1 (ET-1), nitrogen monoxide (NO) and oxytocin receptor (OXTR) levels in the uterine tissues of Sprague-Dawley (SD) rats following abortion. A total of 30 SD rats undergoing complete abortion were randomly divided into ultrasound irradiation and sham irradiation groups (15 rats per group). The rats in the ultrasound irradiation group were treated with low-intensity ultrasound (sound intensity, 2 W/cm2; frequency, 0.8 MHz) for 30 min daily for 5 consecutive days, and those in the sham irradiation group received sham treatment. The uterine tissue was removed to measure the levels of ET-1, NO and OXTR using the enzyme-linked immunosorbent assay and immunohistochemistry, respectively. The ET-1 level in the uterine tissues was significantly higher in the ultrasound irradiation group compared to the sham irradiation group (P<0.05); however, the NO level was similar in the 2 groups (P>0.05). In the uterine myometrium and endometrium, the strong positive expression of OXTR was observed in the ultrasound irradiation group, which was significantly higher compared to the sham irradiation group (P<0.05). Low-intensity ultrasound could promote uterine involution by increasing ET-1 levels, modifying the balance of ET-1 and NO, and enhancing the expression of OXTR in the uterine myometrium and endometrium.

[Effect of low-intensity ultrasound on endothelin-1 and nitrogen monoxide in uterine tissues of SD rats following abortion].

OBJECTIVE: To investigate the effect of low-intensity ultrasound on the contents of endothelin (ET-1) and nitrogen monoxide (NO) in uterine tissues of SD rats after abortion. METHODS: Thirty female pregnant rats were randomly divided into treatment group and control group and received mifepristone and misoprostol to induce abortion. The rats in the treatment group were treated by low-intensity ultrasound for 30 min/day for 5 consecutive days, and those in the control group received sham treatment. The uterine tissue was then taken and homogenized for measurement of ET-1 and NO contents using enzyme-linked immunosorbent assay and chemical testing. RESULTS: ET-1 content in the uterine tissues was significantly higher in the treatment group than in the control group (P<0.05), but NO content showed no significant difference between the two groups (P>0.05). CONCLUSIONS: Low-intensity ultrasound can promote the contraction of uterine smooth muscles by increasing the level of ET-1 to modulate the homeostasis of ET-1 and NO.