SEPT3 as a Potential Molecular Target of Triple-Negative Breast Cancer.

Background: The survival rate for triple-negative breast cancer (TNBC) is very low due to its advanced metastatic and aggressive nature, and there is no specific target to improve the survival rate. The expression and clinical signature of neuronal-specific septin-3 (Septin3, SEPT3) in TNBC remain undetermined. Methods: SEPT3 differential expression in TNBC was detected with the use of bioinformatic approaches based on TCGA and GEO database, which was verified with immunohistochemistry in TNBC tissues. Next, the effect of SEPT3 on survival and the association between SEPT3 expression and clinical characteristics were assessed for TNBC patients. We performed Cox analysis to evaluate whether SEPT3 is an independent predictor for TNBC patients. Results: SEPT3 was identified as a key differentially expressed gene. SEPT3 was observed to be elevated in 112 TNBC significantly. Increased expression of SEPT3 contributed to an unfavorable prognosis in patients with TNBC. Additionally, SEPT3 was associated with several factors including TNM stage, lymph node metastasis, Ki67 level and histological grade. SEPT3 was determined to be an independent risk factor for TNBC patients through Cox regression analysis. Conclusion: This study demonstrated that SEPT3 could be a potential disease marker for TNBC patients by bioinformatics analysis and validation in clinical samples.

Risk factors for post-traumatic stress disorder among young and middle-aged cancer patients in the intensive care unit: A case-control study.

BACKGROUND: Young and middle-aged cancer patients in intensive care unit (ICU) often suffer from stress and pressure, causing huge physical and mental damage. Currently, there is few research on post-traumatic stress disorder (PTSD) among young and middle-aged cancer patients in ICU in China, and the psychological status of patients who have experienced both cancer development and ICU stay is still unclear. AIM: To explore the risk factors for PTSD in young and middle-aged patients with cancer in ICU. METHODS: Using convenient sampling method, we enrolled 150 young and middle-aged patients with cancer who were admitted to the ICU of our center during the period from July to December 2020. The general data of the patients and PTSD-related indicators were collected. The Impact of Event Scale-Revised (IES-R) was used for assessing PTSD one month after the discharge from the ICU. Binary Logistic regression analysis was performed to assess the independent risk factors for PTSD in these patients. RESULTS: Among these 150 patients, 32 (21.33%) were found to be with PTSD. Binary Logistic regression analysis revealed that factors significantly associated with PTSD among young and middle-aged patients with cancer in ICU included monthly income (OR = 0.24, P = 0.02), planned transfers (OR = 0.208, P = 0.019), and Acute Physiology and Chronic Health Evaluation (APACHE II) score (OR = 1.171, P = 0.003). CONCLUSION: The low monthly income, unplanned transfers, and increased APACHE II score are the risk factors for PTSD in young and middle-aged patients with cancer in ICU.

SEPTIN3 Promotes Progression of Triple-Negative Breast Cancer via Activating Wnt Pathway.

Background: There is a lack of targeted therapies for triple-negative breast cancer (TNBC), necessitating the search for novel targets. Patients with TNBC exhibit elevated expression of neuron-specific septin-3 (SEPTIN3), leading to poor prognosis. This study aimed to investigate the modulation of SEPTIN3 expression in TNBC cells. Methods: The relative expression levels of SEPTIN3 in TNBC tissues and cell lines were determined using Western blotting and qRT-PCR. We generated lentivirally transduced TNBC cell lines so such that SEPTIN3 was overexpressed or knocked down. Next, the effect of SEPTIN3 on the biological behavior of TNBC cells was detected using a series of functional assays, including CCK8, colony formation, scratch, and transwell assays. We monitored the tumorigenicity of SEPTIN3 overexpressed cells and performed Ki-67 immunostaining in mice. The mechanism mediated by SEPTIN3 was studied using functional enrichment analysis and Western blotting. Results: Protein and mRNA expression levels of SEPTIN3 were observed to be increased in TNBC tissues and cell lines. SEPTIN3 knockdown reduced cell growth, invasion, and migration, whereas SEPTIN3 overexpression exerted the opposite effects. SEPTIN3 was observed to favor cell growth and tumorigenicity in vivo. In addition, SEPTIN3 promoted TNBC cell aggressiveness and proliferation via activation of the Wnt signaling pathway. Conclusion: SEPTIN3 emerged as an oncogene that accelerates tumor progression by regulating the Wnt signaling pathway.