ABSTRACT
OBJECTIVE: To compare the efficacy and safety of radical surgery with radiotherapy in patients with early-stage cervical carcinoma. METHODS: PubMed, Web of Science, and Embase were systematically reviewed, and studies comparing radical surgery with radiotherapy were included. The main efficacy outcomes included overall survival (OS), and disease-free survival (DFS). Safety endpoints were adverse events. Hazard ratios (HR) or risk ratios (RR) with 95% CI were used to pool the estimates. RESULTS: A total of 6 studies were included in this meta-analysis. Radical surgery was associated with comparable survival effects in OS (HR = 0.73; 95% CI 0.46-1.17; p = 0.196) and DFS (HR = 0.84; 95% CI 0.64-1.10; p = 0.207) as compared with radiotherapy. Moreover, positive lymphangiography (HR = 3.67; 95% CI 2.86-4.70; p < 0.001), adeno-carcinomatous histotype (HR = 2.53; 95% CI 1.80-3.56; p < 0.001), adenosquamous histotype (HR = 1.55; 95% CI 1.27-1.89; p < 0.001), tumor size ≥4 cm (HR = 1.60; 95% CI 1.14-2.23; p < 0.001), stage IB2 (HR = 1.71; 95% CI 1.43-2.04; p < 0.001), and stage IIA (HR = 1.85; 95% CI 1.54-2.22; p < 0.001) were all independent predictors of decreased survival. Patients treated with radical surgery had a rate of adverse events similar to that of those treated with radiotherapy (RR = 1.23; 95% CI 0.61-2.48; p = 0.557). CONCLUSION: The present study suggested that radical surgery and radiotherapy offered similarly effective treatment in terms of OS and DFS in early-stage cervical carcinoma. Moreover, the complication rate between the 2 treatments was not significantly different. Considering the potential limitations of this study, more large-scale well-designed randomized controlled trials are needed to verify our findings.
Subject(s)
Uterine Cervical Neoplasms , Disease-Free Survival , Female , Humans , Hysterectomy , Neoplasm Staging , Progression-Free Survival , Randomized Controlled Trials as Topic , Uterine Cervical Neoplasms/radiotherapy , Uterine Cervical Neoplasms/surgeryABSTRACT
BACKGROUND: Studies have considered long non-coding RNA 5 prime to Xist (lncRNA FTX) a key lncRNA for normal uterine development, but it has not been reported whether lncRNA FTX is involved in regulating the development of endometriosis (EMs). The aim of the present study was to explore the effect and mechanism of long non-coding RNA 5 prime to Xist (lncRNA FTX) on the invasion, metastasis, and epithelial-mesenchymal transition (EMT) of endometrial stromal cells (ESCs) caused by EMs. METHODS: Ectopic or normal endometrial tissues were collected from 38 patients with EMs, who were diagnosed and operated on at Beijing Tongren Hospital from June 2018 to December 2019, and 20 healthy volunteers with normal endometria. The expression of lncRNA FTX in both groups was detected by quantitative reverse transcription polymerase chain reaction. Ectopic endometrial stromal cells (EESC) and ESC from patients with EMs and healthy volunteers were separated and cultured, and the expression of lncRNA FTX in the cells was detected. The expression of lncRNA FTX in EESC was overexpressed or interfered. Proliferation, invasion, and migration was detected by Cell Counting Kit-8, transwell assay, and scratch assay. Apoptosis and cell cycle were detected by flow cytometry. EMT-related protein and PI3K/Akt signaling pathway-related protein expressions were detected by Western blot. RESULTS: LncRNA FTX was underexpressed in endometrial tissues and EESC from patients with EMs. The overexpression of lncRNA FTX could significantly inhibit the proliferation, invasion, and migration of EESC, but promoted apoptosis and cell cycle arrest in the G0/G1 phase. The overexpression of lncRNA FTX significantly increased the expression of EMT-related protein, E-cadherin, and decreased the protein expression of vimentin, N-cadherin, and zinc finger E-box binding homeobox 1. In addition, the overexpression of lncRNA FTX could decrease the expression of p-PI3K/PI3K and p-Akt/Akt. Interfering with the expression of lncRNA FTX had the opposite result. CONCLUSIONS: The overexpression of lncRNA FTX could decrease the invasion, metastasis, and EMT of ESC caused by EMs by inhibiting the activity of the PI3K/Akt signaling pathway.
ABSTRACT
Increased endometrial stromal cell (ESC) survival and migration is responsible for the development and progression of endometriosis. However, little is known about the mechanisms underlying ESC survival and migration, and limited therapeutic strategies that are able to reverse these abnormalities are available. The present study investigated the effects of zearalenone (ZEA) on ESC survival and migration, particularly focusing on mitochondrial fission and the cJun Nterminal kinase (JNK)/dynaminrelated protein 1 (Drp1) pathway. The results revealed that ZEA induced ESC apoptosis in a dosedependent manner. Furthermore, ZEA treatment triggered excessive mitochondrial fission resulting in structural and functional mitochondrial damage, leading to the collapse of the mitochondrial membrane potential and subsequent leakage of cytochrome c into the cytoplasm. This triggered the mitochondrial pathway of apoptosis. Additionally, ZEAinduced mitochondrial fission decreased ESC migration through Factin/Gactin homeostasis dysregulation. ZEA also increased JNK phosphorylation and subsequently Drp1 phosphorylation at the serine 616 position, resulting in Drp1 activation. JNK/Drp1 pathway inhibition abolished the inhibitory effects of ZEA on ESC survival and migration. In summary, the present study demonstrated that ZEA reduced ESC survival and migration through the stimulation of mitochondrial fission by activation of the JNK/Drp1 pathway.
