LIMK1 promotes the development of cervical cancer by up-regulating the ROS/Src-FAK/cofilin signaling pathway.

OBJECTIVE: In this study, we investigated the mechanism of action of LIMK1 in cervical cancer progression. METHODS: The biological role of LIMK1 in regulating the growth, invasion, and metastasis of cervical cancer was studied in SiHa, CaSki cells and nude mice tumor models. The role of LIMK1 in the growth of cervical cancer was evaluated by HE staining. The role of LIMK1 in the invasion, metastasis, and proliferation of cervical cancer was evaluated by cell scratch, Transwell, and monoclonal experiments. The interaction among LIMK1, ROS, and Src was evaluated by Western blotting. The effects of regulating ROS and p-Src expression on LIMK1 in the migration/invasion and proliferation of cervical cancer cells were evaluated through cellular functional assays. RESULTS: Overexpression of LIMK1 promoted tumor growth in nude mice. Cell scratch, Transwell, and monoclonal experiments suggested that LIMK1 promoted the invasion, metastasis, and proliferation of cervical cancer cells. Western blotting suggested that LIMK1 can promote the expression of ROS-related proteins NOX2, NOX4, p-Src, and downstream proteins p-FAK, p-ROCK1/2, p-Cofilin-1, F-actin and inhibit the expression of p-SHP2 protein. Correction experiments showed that LIMK1 regulated the expression of p-FAK and p-Cofilin-1 proteins by regulating ROS and p-Src. Through the detection of cervical cancer cell functions, it was found that the activation of ROS and p-Src induced by LIMK1 is an early event that promotes the migration, proliferation, and invasion of cervical cancer cells. CONCLUSIONS: LIMK1 promotes the expression of F-actin and promotes the development of cervical cancer by regulating the oxidative stress/Src-mediated p-FAK/p-ROCK1/2/p-Cofilin-1 pathway.

A case report of laparoscopic surgery for Mayer-Rokitansky-Küster-Hauser syndrome with preservation of functional primordial uterus.

BACKGROUND: In the past, the primary treatment for MRKH syndrome (Mayer-Rokitansky-Küster-Hauser syndrome) with a functional primordial uterus was surgical removal of the functional primordial uterus. In rare instances, the endometrium of the functional primordial uterus is well developed, and surgical preservation of the functional primordial uterus provides the possibility of preserving reproductive function for these patients. CASE PRESENTATION: A 14-year-old female was diagnosed with type I MRKH syndrome with a functional primordial uterus through physical examination and imaging investigations. We freed the functional primordial uterus through laparoscopic surgery and excised a portion of the lower myometrium to create an outlet at a lower uterine segment, which we then intermittently anastomosed to the tip of the artificial vagina. The patient recovered well after the surgery, and a re-examination showed no significant abnormalities. CONCLUSION: We were successful in preserving the functional primordial uterus using laparoscopic surgery in a patient with MRKH syndrome and connecting it to an artificial vagina through reconstructive surgery to ensure unobstructed menstrual drainage and preserve the reproductive potential of the patient.

Stratifin (SFN) Regulates Cervical Cancer Cell Proliferation, Apoptosis, and Cytoskeletal Remodeling and Metastasis Progression Through LIMK2/Cofilin Signaling.

The aberrant expression of Stratifin (SFN) is intricately associated with the initiation and progression of numerous tumors. This study aims to investigate whether SFN regulates the metastasis of cervical cancer cells through the LIMK2/Cofilin signaling pathway. In this study, we compared the expression of SFN in normal cervical tissues and cervical carcinoma tissues. We established SFN overexpression and SFN silencing cellular models to assess the invasive and migratory capabilities of cervical cancer cells using transwell and scratch assays. YO-PRO-1/PI and EdU staining were employed to evaluate apoptotic and proliferative capacities, while Actin-Tracker Green-488 was utilized to investigate cytoskeletal remodeling. The expression levels of SFN, LIMK2, p-LIMK2, Cofilin, and p-Cofilin were examined through Western blotting and immunofluorescence. Our findings revealed elevated expression of SFN in cervical squamous cell carcinoma tissues. SFN overexpression was observed to enhance invasion and migration of cervical cancer cells, induce cytoskeletal remodeling, facilitate cell proliferation, and suppress apoptosis. Furthermore, SFN overexpression upregulated the expression levels of LIMK2, p-LIMK2, Cofilin, and p-Cofilin. Conversely, silencing SFN exerted opposite effects. SFN plays an important role in the diagnosis of cervical cancer. SFN can regulate cervical cancer cell proliferation, apoptosis, cytoskeletal remodeling and metastasis through LIMK2/Cofilin signaling.

Fast Independent Component Analysis Algorithm-Based Functional Magnetic Resonance Imaging in the Diagnosis of Changes in Brain Functional Areas of Cerebral Infarction.

The aim of this study was to analyze the application value of functional magnetic resonance imaging (FMRI) optimized by the fast independent component correlation algorithm (ICA algorithm) in the diagnosis of brain functional areas in patients with lumbar disc herniation (LDH). An optimized fast ICA algorithm was established based on the ICA algorithm. 50 patients with cerebral infarction were selected as the research objects, and 30 healthy people were selected as the control group. The 50 patients from the observation group were examined by fMRI based on Fast ICA algorithm, while the control group was tested by fMRI based on the routine ICA algorithm. The performances of the two algorithms, the analysis results of the two groups of brain functional areas, cerebral blood flow (CBF), resting state functional connectivity (rsFC), behavioral data, and image data correlation of patients were compared. The results showed that the sensitivity, specificity, and accuracy of Fast ICA algorithm were 97.83%, 89.52%, and 96.27%, respectively, which in the experimental group were greatly better than the control group (88.73%, 72.19%, and 89.72%), showing statistically significant differences (P < 0.05). The maximum Dice coefficient of FAST ICA algorithm was 0.967, and FAST ICA algorithm was better obviously than the traditional ICA algorithm (P < 0.05). The cerebral blood flow of the healthy superior frontal gyrus (SFG) and healthy superior marginal gyrus (SMG) of the observation group with good motor function recovery were 1.02 ± 0.22 and 1.53 ± 0.61, respectively; both indicators showed an increasing trend, and those in the experimental group were much higher in contrast to the control group, showing statistically obvious differences (P < 0.05). Besides, the detection results of cerebral blood flow (CBF) in the healthy SFG and healthy SMG were negatively correlated with the results of connection test B. In summary, the fMRI based on the Fast ICA algorithm showed a good diagnostic effect in the changes of brain functional areas in patients with cerebral infarction. The experimental results showed that the cerebral blood flow in the brain area was related to motor or cognitive function. The results of this study provided a reliable reference for the examination and diagnosis of brain functional areas in patients with cerebral infarction.

PCBP2 promotes the development of glioma by regulating FHL3/TGF-ß/Smad signaling pathway.

The purpose of this study was to investigate the role of Poly (C)-binding protein 2 (PCBP2) and the related signaling pathway in glioma progression. Quantitative real-time polymerase chain reaction (qRT-PCR) and immunohistochemistry (IHC) were performed to measure PCBP2 messenger RNA and protein expression in glioma tissues or cells. Cell transfection was completed using Lipofectamine 2000. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, Transwell assay and flow cytometry assay were used to explore the effects of PCBP2 expression on biological behaviors of glioma cells. Western blot assay was used for the detection of pathway related proteins. Expression of PCBP2 in glioma tissues and cells were higher than that in paracancerous tissues and normal cells (both p < .01). Moreover, the elevated expression of PCBP2 was significantly correlated with tumor size (p = .001) and WHO stage (p = .010). Knockdown of PCBP2 could suppress proliferation, migration and invasion of glioma cells and promote apoptosis. Besides, the expression of transforming growth factor-ß (TGF-ß) pathway related proteins TGF-ß1, p-Smad2 and p-Smad7 were decreased following the downregulation of PCBP2. PCBP2 also inhibited FHL3 expression by binding to FHL3-3'UTR. The inhibition of FHL3 could reverse the antitumor action caused by PCBP2 silencing. In vivo assay, PCBP2 was also found to inhibit the tumor growth of glioma. PCBP2 activates TGF-ß/Smad signaling pathway by inhibiting FHL3 expression, thus promoting the development and progression of glioma.

Evaluation of hippocampal volume and serum brain-derived neurotrophic factor as potential diagnostic markers of conversion from amnestic mild cognitive impairment to Alzheimer disease: A STROBE-compliant article.

Amnestic mild cognitive impairment (aMCI) is a transitional stage between normal aging and Alzheimer disease (AD), and is associated with an increased risk of AD. Many studies have shown that apolipoprotein E epsilon 4 (APOE ε4) genotype is a major genetic predictor of AD progression, especially in patients with aMCI. However, the application of APOE genotyping in the diagnosis of MCI progressing to AD is limited by its low sensitivity and specificity, which often leads to high false-positive rate. The aim of this study was to evaluate serum brain-derived neurotrophic factor (BDNF) and hippocampal volume as predictors of aMCI to AD transition in APOE ε4 genotype patients.A total of 178 subjects were diagnosed with aMCI. The patients with aMCI that progressed to AD within 2 years were included in the MCI-AD group (n = 86), those maintaining an aMCI diagnosis after 2 years were placed in the MCI-MCI group (n = 92), and neurologically healthy age-matched individuals were set as controls (n = 90). APOE genotypes were determined. Blood samples from all subjects were drawn at baseline, 12 months, and 24 months for serum BNDF assessments. Hippocampal delineations were monitored by magnetic resonance imaging.Compared to control group, aMCI-AD patients (the patients with aMCI that progressed to AD within 2 years) exhibited worse performance on cognitive and neuropsychological batteries. Meanwhile, we found that aMCI-AD patients were associated with abnormally low serum BDNF level and greater hippocampal volume loss than MCI-MCI patients (patients maintaining an aMCI diagnosis after 2 years). Moreover, patients with aMCI who were carriers of APOE ε4 showed a notable decrease in serum BDNF and a significant reduction in hippocampal volume, especially in those who progressed to AD.The present study demonstrates that aMCI that evolves into AD in patients with the APOE ε4 genotype may be predicted by hippocampal volume and serum BDNF.