The effects of surgical resection in the treatment of limited-stage small cell lung cancer: a multicenter retrospective study.

This study aimed to examine the effects of surgical resection on the treatment of limited-stage small cell lung cancer and identify patient characteristics that may indicate a benefit from surgical resection. We retrospectively reviewed medical data from patients diagnosed with small cell lung cancer between January 2013 and December 2020 at three hospitals. A total of 478 patients were included in the study, 153 patients received surgery treatment and 325 patients received non-surgery treatment. Survival differences between the surgical resection group and the nonsurgical resection group were analyzed using the Kaplan-Meier method and the log-rank test. The overall survival in the surgical resection group was significantly improved compared to that in the nonsurgical resection group (HR: 0.58, 95% CI: 0.370-0.876, p = 0.0126). Surgical resection significantly improved overall survival compared to nonsurgical resection in stage I disease (HR: 0.56, 95% CI: 0.34-0.94, p = 0.029) and stage IIA disease (HR: 0.60, 95% CI: 0.40-0.92, p = 0.019). However, no significant differences in overall survival were found between surgical resection and nonsurgical resection in stage IIB disease (HR: 0.86, 95% CI: 0.57-1.29, p = 0.46) and stage III disease (HR: 0.99, 95% CI: 0.71-1.39, p = 0.97). The overall survival of patients who underwent lobectomy was significantly better than that of patients who underwent sublobular resection (HR: 1.85, 95% CI: 1.15-4.16, p = 0.021) and who underwent pneumonectomy (HR: 2.04, 95% CI: 1.29-5.28, p = 0.009). Surgical resection should be recommended for patients diagnosed with stage I-IIA SCLC. When deciding on the surgical type, it is preferable to choose lobectomy over sublobar resection or pneumonectomy.

CCT8 promotes cell migration and tumor metastasis in lung adenocarcinomas.

Chaperonins, which contain t-complex polypeptide 1 (CCT), are critical for correct protein folding to generate stable and functional protein conformations, which are important for cell growth and survival. However, little is known about the expression and prognostic significance of CCT8 (subunit 8 of the CCT complex chaperonin) in lung cancer. In this study, we demonstrated that CCT8 expression is frequently increased in human lung cancer. Survival analysis indicated that CCT8 expression is closely correlated with inferior overall survival in lung adenocarcinoma (LUAD), but not in lung squamous carcinoma (LUSC). Subsequently, ectopic expression of CCT8 facilitated cell migration and tumor metastasis, and vice versa. Mechanistically, CCT8 interacted and activated ATK. Inhibition of AKT suppressed CCT8-induced cell migration and tumor metastasis. Our findings support CCT8 as a biomarker for LUAD prognosis and as a target for LUAD therapy.

Serum THBS2 is a potential biomarker for the diagnosis of non-small cell lung cancer.

OBJECTIVE: This study primarily aimed to analyze the levels of THBS2 in the serum of patients diagnosed with non-small cell lung cancer (NSCLC), and subsequently evaluate its potential as a diagnostic biomarker for NSCLC. METHODS: Serum samples were collected from 150 diagnosed NSCLC patients and 150 healthy individuals. The THBS2 concentration in these samples was determined using an enzyme-linked immunosorbent assay (ELISA). The study also investigated the correlation between THBS2 levels and various clinicopathological characteristics in NSCLC patients. The diagnostic sensitivity and specificity of serum THBS2 for NSCLC were assessed using receiver operating characteristic (ROC) curves and their corresponding area under the curve (AUC). RESULTS: Serum THBS2 levels in NSCLC patients were significantly elevated compared to those in healthy individuals. THBS2 levels showed a significant correlation with tumor differentiation grade, tumor size, TNM stage, lymph node metastasis, and distant metastasis. No significant correlation was identified between serum THBS2 levels and other parameters such as gender, age, height, weight, BMI, smoking history, and tumor histological type. At a cutoff value of 7.62 ng/mL, THBS2 could effectively differentiate NSCLC patients from healthy individuals, with a sensitivity of 85.31% and a specificity of 88.92%. The AUC for NSCLC diagnosis using THBS2 was 0.812, significantly surpassing the performance of traditional tumor markers tested, including CEA (0.728), and CYFRA 21­1 (0.685). CONCLUSIONS: Elevated serum THBS2 levels in NSCLC patients suggest its potential as a novel and reliable diagnostic biomarker for NSCLC. Its superior diagnostic performance could potentially outperform traditional tumor markers, leading to improved patient outcomes.

LncRNA BBOX1-AS1 Contributes to the Progression of Esophageal Carcinoma by Targeting the miR-361-3p/COL5A1 Axis.

Long noncoding RNAs (lncRNAs) are known to participate in the progression of several cancers, including esophageal carcinoma (EC), a common malignancy of the digestive system. Although the role of the lncRNA-miRNA-mRNA regulatory network is crucial for the growth and progression of EC, the regulation of lncRNA BBOX1-AS1 (BBOX1 antisense RNA1) remains unclear. We performed reverse transcription-quantitative PCR (RT-qPCR) and western blotting to evaluate miR-361-3p, collagen type V alpha 1 chain (COL5A1), and BBOX1-AS1 expression levels in EC cells and tissues. The colony formation assay (CFA) and Cell Counting Kit-8 (CCK-8) were employed to identify EC cell proliferation, while western blotting was used to examine EC cell apoptosis and Bax and Bcl-2 expression levels. The effect of BBOX1-AS1 on EC proliferation was determined using an in vivo carcinogenesis assay. Correlation between COL5A1, BBOX1-AS1, and miR-361-3p was examined using the luciferase reporter system and RNA immunoprecipitation assay (RIP). Herein, we observed that BBOX1-AS1 expression levels were upregulated in EC cells and tissues. BBOX1-AS1 knockdown inhibited EC cell proliferation and conferred a pro-apoptotic effect. These results indicated a positive interaction between BBOX1-AS1 and miR-361-3p in EC and a negative association with miR-361-3p. COL5A1 was recognized as a downstream miR-361-3p target and was inversely related to miR-361-3p in EC. Therefore, BBOX1-AS1 expression suppressed cell apoptosis and promoted cell proliferation via the downregulation of miR-361-3p and upregulation of COL5A1 expression. Overall, BBOX1-AS1 facilitates EC progression via the miR-361-3p or COL5A1 axis, indicating that BBOX1-AS1 might be a potential therapeutic target for EC therapy.

LncRNA BBOX1-AS1 targets miR-361-3p/COL1A1 axis to drive the progression of oesophageal carcinoma.

BACKGROUND: Oesophageal carcinoma (EC) is one of the types of prevalent malignant cancer in the globe. Many researchers reported the vital role played by long-coding RNAs in EC. In the current research, we investigated the mechanisms of the action of lncRNA BBOX1-AS1 in EC progression. METHODS: In EC tissues and EC cells, the expression levels of miR-361-3p along with COL1A1 and BBOX1-AS1 were detected through RT-qPCR or western blotting. MiR-361-3p interactions with BBOX1-AS1 or COL1A1 were verified through Luciferase reporter and RIP tests. Loss of function combined with caspase-3 activity, CCK-8 and Transwell assays was performed to investigate cell apoptosis, proliferation and migration, respectively. Knockdown of BBOX1-AS1 was used for evaluating BBOX1-AS1 effects on tumour development in vivo. RESULTS: BBOX1-AS1 was remarkably elevated in EC tissues and cells. In addition, the silencing of BBOX1-AS1 attenuated the cell viability, cell migration and enhanced cell apoptosis of EC, as well as suppressed EC tumour formation in vivo. Moreover, BBOX1-AS1 was found to be a sponge of miR-361-3p, which downregulated miR-361-3p expression. MiR-361-3p inhibitor rescued the anti-tumour effect of BBOX1-AS1 knockdown on the progression of EC. Furthermore, we discovered that miR-361-3p specially bound to COL1A1 3'UTR and downregulated COL1A1 and COL1A1 reduction declined the promoting effect of silencing miR-361-3p on EC cell malignant phenotypes. CONCLUSION: BBOX1-AS1 facilitated the EC development and malignancy via miR-361-3p/COL1A1 axis, indicating BBOX1-AS1 could be a novel therapy target for the diagnostic of EC.

The Effect of miR-505-5p on Inhibition of Serum Uromodulin Ameliorates Myocardial Inflammation and Apoptosis Induced by Ischemia-Reperfusion.

Background: It has been found that miR-505-5p is closely related to cardiovascular metabolic risk factors. Nonetheless, there is little research analyzing miR-505-5p for its role as well as molecular mechanism in myocardial injury caused by ischemia-reperfusion (I/R). Methods: This work utilized quantitative reverse transcriptase PCR (qRT-PCR) for detecting miR-505-5p and serum uromodulin (sUmod) levels. sUmod, interleukin-1beta (IL-1ß), IL-6, IL-10, caspase7, caspase9, tumor necrosis factor-alpha (TNF-α), Bax, and Bcl-xL expression was detected by western blot. Bioinformatics database was used for target prediction and miR-505-5's target was determined by luciferase reporter gene assay. Results: Relative to sham group, sUmod was highly expressed within myocardial I/R injury (MIRI), whereas sUmod silencing significantly decreased the heart weight/body weight ratio, reduced serum myocardial enzymes expression, ameliorated I/R-mediated myocardial apoptosis, and inflammation. TargetScan bioinformatics database and luciferase reporter genes confirmed that sUmod was miR-505-5p's direct target gene, besides, miR-505-5p overexpression significantly improved the myocardial injury score, increased IL-10, decreased TNF-α, IL-1ß, IL-6 expression, decreased caspase7, caspase9, Bax expression, and increased Bcl-xL expression. More importantly, overexpression of sUmod abolished miR-505-5p overexpression's role in I/R-mediated myocardial apoptosis and inflammation. Conclusion: miR-505-5p can improve I/R-mediated myocardial apoptosis and inflammation by targeting sUmod. In this study, miR-505-5p is related to MIRI pathogenesis, which provides the new possible targeted therapy in patients with MIRI.