Application of Chest CT Imaging Feature Model in Distinguishing Squamous Cell Carcinoma and Adenocarcinoma of the Lung.

Purpose: In situations where pathological acquisition is difficult, there is a lack of consensus on distinguishing between adenocarcinoma and squamous cell carcinoma from imaging images, and each doctor can only make judgments based on their own experience. This study aims to extract imaging features of chest CT, extract sensitive factors through logistic univariate and multivariate analysis, and model to distinguish between lung squamous cell carcinoma and lung adenocarcinoma. Methods: We downloaded chest CT scans with clear diagnosis of adenocarcinoma and squamous cell carcinoma from The Cancer Imaging Archive (TCIA), extracted 19 imaging features by a radiologist and a thoracic surgeon, including location, spicule, lobulation, cavity, vacuolar sign, necrosis, pleural traction sign, vascular bundle sign, air bronchogram sign, calcification, enhancement degree, distance from pulmonary hilum, atelectasis, pulmonary hilum and bronchial lymph nodes, mediastinal lymph nodes, interlobular septal thickening, pulmonary metastasis, adjacent structures invasion, pleural effusion. Firstly, we apply the glm function of R language to perform logistic univariate analysis on all variables to select variables with P < 0.1. Then, perform logistic multivariate analysis on the selected variables to obtain a predictive model. Next, use the roc function in R language to calculate the AUC value and draw the ROC curve, use the val.prob function in R language to draw the Calibrat curve, and use the rmda package in R language to draw the DCA curve and clinical impact curve. At the same time, 45 patients diagnosed with lung squamous cell carcinoma and lung adenocarcinoma through surgery or biopsy in the Radiotherapy Department and Thoracic Surgery Department of our hospital from 2023 to 2024 were included in the validation group. The chest CT features were jointly determined and recorded by the two doctors mentioned above and included in the validation group. The included image feature data are complete and does not require preprocessing, so directly entering statistical calculations. Perform ROC curves, calibration curves, DCA, and clinical impact curves in the validation group to further validate the predictive model. If the predictive model performs well in the validation group, further draw a nomogram to demonstrate. Results: This study extracted 19 imaging features from the chest CT scans of 75 patients downloaded from TCIA and finally selected 18 complete data for analysis. First, univariate analysis and multivariate analysis were performed, and a total of 5 variables were obtained: spicule, necrosis, air bronchogram Sign, atelectasis, pulmonary hilum and bronchial lymph nodes. After conducting modeling analysis with AUC = 0.887, a validation group was established using clinical cases from our hospital, Draw ROC curve with AUC = 0.865 in the validation group, evaluate the accuracy of the model through Calibrate calibration curve, evaluate the reliability of the model in clinical practice through DCA curve, and further evaluate the practicality of the model in clinical practice through clinical impact curve. Conclusion: It is possible to extract influential features from ordinary chest CT scans to determine lung adenocarcinoma and squamous cell carcinoma. The model we have set up performs well in terms of discrimination, accuracy, reliability, and practicality.

A Clinical Study on Video Bronchoscopy-guided Coblation for Benign Central Airway Stenosis.

Background: Benign central airway stenosis poses a significant challenge to respiratory and thoracic surgeons due to the high recurrence rate associated with current treatment methods, causing severe breathing difficulties and potentially life-threatening complications. This article aims to investigate the therapeutic efficacy and prospects of using coblation in the management of benign central airway stenosis in adults. Moreover, the pathogenesis of benign central airway stenosis was deeply explored to provide better guidance for future clinical treatments. Materials and Methods: This retrospective study examined patients with benign central airway stenosis who were treated at The Second Hospital of Hebei Medical University from 2017 to 2020. In addition, a comparative analysis of whole-genome sequencing was conducted between the aforementioned patient group and healthy populations to investigate the underlying etiology of this stenotic condition. Results: The present study encompassed 32 patients who underwent 43 treatments in total between 2017 and 2020. All patients exhibited alleviation of airway stenosis and an improvement in clinical symptoms following surgery, without any significant surgical or postoperative complications. Whole-genome analysis revealed significant changes in gene expression in the airway mucosa of patients with benign airway stenosis in comparison to healthy populations. A total of 91 differentially expressed genes were identified, among which 44 upregulated genes displayed characteristics of promoting inflammatory responses. Conclusion: Coblation demonstrates promise as an efficacious treatment modality for adults suffering from benign central airway stenosis, and its widespread application in clinical settings is anticipated. The direct pathogenesis of benign central airway stenosis involves airway lumen narrowing and obstruction resulting from excessive inflammation and proliferative granulation.

Mechanistic Insights into the Biodegradation of Carbon Dots by Fungal Laccase.

While carbon dots (CDs) have the potential to support the agricultural revolution, it remains obscure about their environmental fate and bioavailability by plants. Fungal laccase-mediated biotransformation of carbon nanomaterials has received little attention despite its known capacity to eliminate recalcitrant contaminants. Herein, we presented the initial investigation into the transformation of CDs by fungal laccase. The degradation rates of CDs were determined to be first-order in both substrate and enzyme. Computational docking studies showed that CDs preferentially bonded to the pocket of laccase on the basal plane rather than the edge through hydrogen bonds and hydrophobic interactions. Electrospray ionization-Fourier transform-ion cyclotron resonance mass spectrometry (ESI-FT-ICR MS) and other characterizations revealed that the phenolic/amino lignins and tannins portions in CDs are susceptible to laccase transformation, resulting in graphitic structure damage and smaller-sized fragments. By using the 13C stable isotope labeling technique, we quantified the uptake and translocation of 13C-CDs by mung bean plants. 13C-CDs (10 mg L-1) accumulated in the root, stem, and leaf were estimated to be 291, 239, and 152 µg g-1 at day 5. We also evidenced that laccase treatment alters the particle size and surface chemistry of CDs, which could facilitate the uptake of CDs by plants and reduce their nanotoxicity to plants.

Curcumin increases crizotinib sensitivity through the inactivation of autophagy via epigenetic modulation of the miR-142-5p/Ulk1 axis in non-small cell lung cancer.

Drug resistance is a critical factor responsible for the recurrence of non-small cell lung cancer (NSCLC). Previous studies suggest that curcumin acts as a chemosensitizer and radiosensitizer in human malignancies, but the underlying mechanism remains elusive. In the present study, we explored how curcumin regulates the expression of miR-142-5p and sensitizes NSCLC cells to crizotinib. We found that miR-142-5p is significantly downregulated in NSCLC tissue samples and cell lines. Curcumin could increase crizotinib cytotoxicity by epigenetically restoring the expression of miR-142-5p. Furthermore, curcumin treatment suppressed the expression of DNA methylation-related enzymes, including DNMT1, DNMT3A, and DNMT3B, in NSCLC cells. In addition, the upregulation of miR-142-5p expression increased crizotinib cytotoxicity and induced apoptosis in tumor cells in a similar manner to that of curcumin. Strikingly, miR-142-5p overexpression suppressed crizotinib-induced autophagy in A549 and H460 cells. Mechanistically, miR-142-5p inhibited autophagy in lung cancer cells by targeting Ulk1. Overexpression of Ulk1 abrogated the miR-142-5p-induced elevation of crizotinib cytotoxicity in A549 and H460 cells. Collectively, our findings demonstrate that curcumin sensitizes NSCLC cells to crizotinib by inactivating autophagy through the regulation of miR-142-5p and its target Ulk1.

miR-365a-5p suppresses gefitinib resistance in non-small-cell lung cancer through targeting PELI3.

Aim: Demonstrate the function of dysregulated miR-365a-5p-PELI3 signaling axis in the generation of gefitinib resistance during treatment for non-small-cell lung cancer (NSCLC). Patients & methods: All the NSCLC patients who participated in this research were recruited from the Second Hospital of Hebei Medical University. PC9 cells and PC9GR cells were cultured for in vitro experiments. Results: Patients who were primary resistant to EGFR-tyrosine kinase inhibitor had lower miR-365a-5p levels. MiR-365a-5p directly targeted PELI3 mRNA. MiR-365a-5p overexpression enhanced the function of gefitinib in inhibiting cell viability. Tumor growth was suppressed through miR-365a-5p in nude mice. Conclusion: Dysregulated miR-365a-5p-PELI3 signaling axis triggered the generation of gefitinib resistance in NSCLC.

Long Non-coding RNA MIAT Mediates Non-small Cell Lung Cancer Development Through Regulating the miR-128-3p/PELI3 Axis.

In this study, we set out to characterize the expression status of long non-coding RNA (lncRNA) Myocardial Infarction Associated Transcript (MIAT) in non-small cell lung cancer (NSCLC) and elucidate its mechanistic contribution to this disease. Relative expression levels of MIAT, Pellino E3 Ubiquitin Protein Ligase Family Member 3 (PELI3), and microRNA (miR)-128-3p were analyzed by real-time polymerase chain reaction. PELI3 protein level was determined by immunoblotting. Cell viability and proliferation were evaluated by the MTT assay and colony formation assay, respectively. Cell invasion and migration were assessed by wound-healing closure and transwell assays, respectively. The regulatory actions of miR-128-3p on both MIAT and PELI3 were interrogated by luciferase reporter assay. We demonstrated the aberrant upregulation of MIAT in NSCLC and its association with tumor progression. We further uncovered the negative correlation among MIAT, PELI3, and miR-128-3p. MIAT deficiency significantly compromised cell viability, proliferation, invasion, and migration, while increased miR-128-3p and decreased PELI3 expressions. Application of miR-128-3p inhibitor significantly stimulated luciferase activities driven by both MIAT and PELI3 promoter and phenotypically promoted cell viability, proliferation, migration, and invasion. Our study highlighted the mechanistic contribution of the MIAT/miR-128-3p/PELI3 signaling cascade in NSCLC.

PELI3 mediates pro-tumor actions of down-regulated miR-365a-5p in non-small cell lung cancer.

BACKGROUND: To analyze the relative expression of PELI3 and its mechanistic involvement in the non-small cell lung cancer (NSCLC). METHODS: PELI3 expression in NSCLC tissue samples was determined by the immunohistochemistry. The transcripts abundance of PELI3 was measured with real-time PCR. The protein intensity was analyzed by western blot. The overall survival in respect to PELI3 or miR-365a-5p expression was plotted by the Kaplan-Meier's analysis. Cell growth was determined by colony formation assay. Cell viability was measured by MTT assay. The migration and invasion were evaluated by wound healing and transwell assay respectively. The regulatory effect of miR-365a-5p on PELI3 was interrogated with luciferase reporter assay. The direct binding between miR-365a-5p and PELI3 was analyzed by pulldown assay. RESULTS: PELI3 was aberrantly up-regulated in NSCLC both in vivo and in vitro. High level of PELI3 associated with poor prognosis. PELI3-deficiency significantly inhibited cell viability, colony formation, migration and invasion. We further identified that miR-365a-5p negatively regulated PELI3 in this disease. Ectopic expression of miR-365a-5p in both A549 and H1299 phenocopied PELI3-deficiency. Meanwhile, PELI3-silencing significantly abolished the pro-tumoral effect elicited by miR-365a-5p inhibition. CONCLUSION: Our results highlighted the importance of dysregulated miR-365a-5p-PELI3 signaling axis in NSCLC.

PELI3 mediates pro-tumor actions of down-regulated miR-365a-5p in non-small cell lung cancer

BACKGROUND: To analyze the relative expression of PELI3 and its mechanistic involvement in the non-small cell lung cancer (NSCLC). Methods: PELI3 expression in NSCLC tissue samples was determined by the immunohistochemistry. The transcripts abundance of PELI3 was measured with real-time PCR. The protein intensity was analyzed by western blot. The overall survival in respect to PELI3 or miR-365a-5p expression was plotted by the Kaplan-Meier's analysis. Cell growth was determined by colony formation assay. Cell viability was measured by MTT assay. The migration and invasion were evaluated by wound healing and transwell assay respectively. The regulatory effect of miR-365a-5p on PELI3 was interrogated with luciferase reporter assay. The direct binding between miR-365a-5p and PELI3 was analyzed by pulldown assay. RESULTS: PELI3 was aberrantly up-regulated in NSCLC both in vivo and in vitro. High level of PELI3 associated with poor prognosis. PELI3-deficiency significantly inhibited cell viability, colony formation, migration and invasion. We further identified that miR-365a-5p negatively regulated PELI3 in this disease. Ectopic expression of miR-365a-5p in both A549 and H1299 phenocopied PELI3-deficiency. Meanwhile, PELI3-silencing significantly abolished the pro-tumoral effect elicited by miR-365a-5p inhibition. CONCLUSIONS: Our results highlighted the importance of dysregulated miR-365a-5p-PELI3 signaling axis in NSCLC.

Biological effects and clinical characteristics of microRNA-106a in human colorectal cancer.

MicroRNAs serve important roles in various diseases, particularly cancer. microRNA-106a (miR-106a) exhibits abnormal expression and oncogenic activity in carcinogenesis. The clinical significance of the abnormal expression of miR-106a in colorectal cancer is poorly understood. In the present study, miR-106a expression from colorectal cancer tissues was quantified using the reverse transcription-quantitative polymerase chain reaction. The overexpression or knockdown of miR-106a was performed by transfection with microRNA mimic or inhibitor in human colorectal carcinoma HCT116 cells. The overexpression of miR-106a promoted viability and inhibited apoptosis in colorectal cancer cells. The association between miR-106a expression and clinicopathological factors was analyzed, and it was identified that miR-106a exhibited significantly increased expression in adenocarcinoma tissues compared with in mucinous carcinoma tissues, and the expression of miR-106a was identified to be associated with the depth of invasion and differentiation. The expression of miR-106a in plasma was also determined and it was identified that increased expression of miR-106a, as a characteristic of patients with colorectal cancer, may be distinguished from that of other patients by digitization of the areas under the receiver operating characteristic curves. These data suggested that miR-106a is a potential biomarker in the diagnosis of colorectal carcinoma. However, the underlying molecular mechanism of miR-106a-promoted viability and inhibition of apoptosis requires further investigation.

Dickkopf-1 is oncogenic and involved in invasive growth in non small cell lung cancer.

Dickkopf-1 (DKK1) is an inhibitor of the Wnt/ß-catenin signaling pathway. However, the role of DKK1 in the progression of non small cell lung cancer (NSCLC) is not fully understood. In this study, RT-PCR and Western blot were used to examine the expression of DKK1 in a panel of ten human NSCLC cell lines and NSCLC tissues. DKK1 expression was highly transactivated in the great majority of these cancer lines. The expression of DKK1 was upregulated on both mRNA and protein levels in NSCLC tissues compared with the adjacent normal lung tissues. Immunohistochemistry and immunofluoresence revealed that DKK1 was mainly distributed in the cytoplasm in both carcinoma tissues and cell lines. DKK1 protein expression was also evaluated in paraffin sections from 102 patients with NSCLC by immunohistochemistry, and 65(63.73%)tumors were DKK1 positive. Relative analysis showed a significant relationship between DKK1 positive expression and lymph node metastasis(P<0.05). Patients with DKK1-positive tumors had poorer DFS than those with negative ESCC (5-year DFS; 15.4% versus 27%, P = 0.007). To further explore the biological effects of DKK1 in NSCLC cells, we over-expressed DKK1 in NSCLC 95C cell using eukaryotic expression vector pCMV-Tab-2b and performed a knockdown of DKK1 in LTEP-a-2 cell using a short hairpin RNA expression vector pSilencer 5.1. DKK1 did not have any effect on proliferation, but seemed to play a role in migration and invasion capability. Overexpression of DKK1 promotes migratory and invasive activity of 95C, while DKK1 knockdown resulted in the suppression of migration and invasion potentials of LTEP-a-2 cell. Taken together, these results indicate that DKK1 may be a crucial regulator in the progression of NSCLC. DKK1 might be a potential therapeutic target in NSCLC.