During tumor formation and expansion, increasing glucose metabolism is necessary for unrestricted growth of tumor cells. Expression of key glycolytic enzyme alpha-enolase (ENO1) is controversial and its modulatory mechanisms are still unclear in non-small cell lung cancer (NSCLC). The expression of ENO1 was examined in NSCLC and non-cancerous lung tissues, NSCLC cell lines, and immortalized human bronchial epithelial cell (HBE) by quantitative real-time reverse transcription PCR (qRT-PCR), immunohistochemistry, and Western blot, respectively. The effects and modulatory mechanisms of ENO1 on cell glycolysis, growth, migration, invasion, and in vivo tumorigenesis and metastasis in nude mice were also analyzed. ENO1 expression was increased in NSCLC tissues in comparison to non-cancerous lung tissues. Similarly, NSCLC cell lines A549 and SPCA-1 also express higher ENO1 than HBE cell line in both mRNA and protein levels. Overexpressed ENO1 significantly elevated NSCLC cell glycolysis, proliferation, clone formation, migration, and invasion in vitro, as well as tumorigenesis and metastasis in vivo by regulating the expression of glycolysis, cell cycle, and epithelial-mesenchymal transition (EMT)-associated genes. Conversely, ENO1 knockdown reversed these effects. More importantly, our further study revealed that stably upregulated ENO1 activated FAK/PI3K/AKT and its downstream signals to regulate the glycolysis, cell cycle, and EMT-associated genes. This study showed that ENO1 is responsible for NSCLC proliferation and metastasis; thus, ENO1 might serve as a potential molecular therapeutic target for NSCLC treatment.

Oleanolic acid (OA), a compound known for its potent antitumour properties, has been the subject of investigations in both cell and animal models. Although OA has good biological activity, its low water solubility and bioavailability limit its therapeutic use, and therefore translating the potential of OA into the clinical oncology setting remains challenging. The present systematic review and meta‑analysis utilized evidence from animal model studies to gain insights into the antitumour mechanisms of OA to address the gap in understanding, and to provide guidance for future research directions and potential clinical applications. The guidelines outlined in the Preferred Reporting Items for Systematic Reviews and Meta‑Analyses were applied in the present study and a comprehensive search was conducted across the PubMed/MEDLINE, Web of Science, Cochrane Library and Embase databases, with a cut‑off date of June 30, 2023. The primary focus was on randomized controlled trials that used animal models to assess the antitumour effects of OA. The methodological quality appraisal was conducted using the Systematic Review Centre for Laboratory Animal Experimentation risk of bias tool, and tumour volume and weight served as the principal outcome measures. Data were analysed using the RevMan (version 5.3) and Stata SE11 software packages, with an assessment of heterogeneity conducted using the I² statistical test, sensitivity analysis conducted using the leave‑one‑out approach, and evaluation of publication bias performed using Egger's test and funnel plot analysis. The present study demonstrated a significant inhibitory effect of OA intervention on tumour growth and a decrease in tumour weight in animal models. Despite the broad spectrum of antitumour effects exhibited by OA, further investigations are warranted to optimize the dosage and administration routes of OA to maximize its efficacy in clinical cancer treatment.

Cisplatin (DDP) is the principal agent used for chemotherapy in patients with non-small cell lung cancer (NSCLC). Nevertheless, DDP resistance is an essential cause for a worse prognosis of patient. Therefore, this study proposes to discover features of miR-424-5p in DDP resistance of NSCLC. After exogenous modulation of miR-424-5p expression, A549 cell activity was measured using CCK-8 and flow cytometry. A549/DDP and A549/DDP-associated subcutaneous tumor model were constructed to investigate the effect of miR-424-5p on DDP resistance in NSCLC in vivo. TargetScan and JASPAR databases predicted the potential molecular mechanism of miR-424-5p. A549-and A549/DDP-derived exosomes were isolated and characterized using a transmission electron microscope and nanoparticle tracking analysis. Overexpression of miR-424-5p facilitated proliferation and DDP resistance in A549 cells, and knockdown of miR-424-5p did the opposite. Knockdown of miR-424-5p enhanced DDP restriction on tumor weight and volume. Moreover, SOCS5 and SOCS56 (SOCS5/6) were downstream targets of miR-424-5p. miR-424-5p down-regulated SOCS5/6 expression to activate JAK2/STAT3 and PI3K/AKT pathways. Notably, tumor protein p53 (TP53) is a transcription factor for the miR-424-5p host gene, as confirmed by the dual-luciferase reporter gene. Cellular and animal experiments indicated that TP53 limited the regulatory function of miR-424-5p on NSCLC growth, DDP resistance, and related molecules. Interestingly, miR-424-5p was markedly enriched in A549/DDP cell-derived exosomes than in A549 cell-derived exosomes, and TP53 down-regulated miR-424-5p expression in A549/DDP cell-derived exosomes. DDP-resistant cell-derived exosome miR-424-5p contributes to NSCLC growth and DDP resistance by targeting SOCS5 and SOCS6 to activate JAK2/STAT3 and PI3K/AKT pathways, which are blocked by TP53.

We aimed to investigate the potential of phenethyl isothiocyanate (PEITC) as an effective therapeutic agent in overcoming cisplatin resistance in non-small cell lung cancer (NSCLC). Cell viability was measured using the CCK-8 assay and flow cytometry, and a xenograft model was established to verify the antitumor effect of PEITC on A549/DDP cells. The JASPAR database was used to predict the potential molecular mechanisms. Mechanistic exploration was conducted using Western blot and qRT-PCR analyses, and predictions were validated with a dual-luciferase reporter assay. The findings show that PEITC treatment led to decreased cell proliferation, increased apoptosis, and cessation of cell cycle progression at G1 phase. PEITC inhibited tumor growth in a concentration-dependent manner in a mouse xenograft model. Examination of the possible mechanism of PEITC showed that this compound led to down-regulation of miR-424-5p and c-Myc, up-regulation of suppressor of cytokine signaling 5/6 (SOCS5/6), and down-regulation of AKT/PI3K/mTOR signaling. A dual-luciferase reporter assay showed that miR-424-5p targeted c-Myc, and that silencing of c-Myc decreased the expression of downstream genes. These results suggest that PEITC inhibited the growth and increased the sensitivity of cisplatin-resistant NSCLC cells by targeting c-Myc and down-regulating the PI3K/AKT/mTOR pathway. Clinical trial number: not applicable.

Background Primary lung carcinosarcoma, characterized by the presence of both carcinoma and sarcoma components, is a rare soft tissue malignancy. Its pathogenesis remains incompletely elucidated, and it exhibits significant resistance to conventional therapeutic interventions, resulting in a dismal prognosis. Consequently, there is currently no established standard treatment protocol for lung carcinosarcoma, leading most clinicians to draw upon their experiences with other tumor types when formulating treatment strategies. Case description A 56-year-old non-smoking male presented with a progressively enlarging mass in the right cervical region, The diagnosis of lung carcinosarcoma was definitively confirmed through CT-guided biopsy. First-line immunotherapy combined with targeted therapy was ineffective; second-line chemotherapy was effective, chest CT revealed the disappearance of enlarged lymph nodes in the retrosternal area and a significant reduction of pulmonary lesions, but showed signs of brain metastasis. the patient passed away at home on June 27th, 2023 due to sudden onset dyspnea accompanied by loss of consciousness. Literature review A comprehensive literature search for lung carcinosarcoma was conducted across four databases, including PubMed/MEDLINE, Web of Science, Cochrane Library, and Embase, covering the period from 1968 to 2023. A total of 48 patients were included for analysis. Further survival analysis revealed a median survival time of 18 months; adjuvant therapy following surgery significantly improved survival compared to surgery alone and other treatment modalities. Conclusion Lung carcinosarcoma is an exceptionally rare malignant neoplasm of the lung, and definitive treatment protocols remain elusive. The most effective strategy to enhance prognosis may still entail complete surgical resection of the lesions in conjunction with adjuvant therapy.

Background Medulloblastoma (MB) is a highly aggressive tumor originating in the cerebellum, predominantly affecting children. Adult medulloblastoma is rare, leading to a lack of a standardized treatment protocol. Although multimodal strategies from pediatric MB have improved outcomes in adult patients, challenges persist, including early diagnosis difficulties, treatment toxicity, recurrence risks, targeted therapies, and controversies over chemotherapy timing and regimen. Case description We present a clinical case involving a 53-year-old male patient diagnosed with multifocal medulloblastoma, who presented with symptoms of dizziness. Cranial magnetic resonance imaging (MRI) revealed space-occupying lesions in the right cerebellar infratentorial region and the right temporal pole, which were initially suspected to be meningiomas. The patient subsequently underwent surgical resection of the subtentorial lesion, which was pathologically confirmed to be a medulloblastoma. Molecular classification through genetic testing classified it as the SHH subtype. Postoperatively, the patient received sequential radiotherapy and chemotherapy. After radiotherapy, the lesion in the temporal pole disappeared, and the patient recovered well. Disease-free survival of this patient was more than 2 years, during which the patient returned to the hospital for follow-up every three months. Currently, the patient is in good condition with no significant treatment sequelae or signs of recurrence. Conclusion Adult medulloblastoma is rare, and adult multifocal medulloblastoma is even rarer. The adult patient with multifocal medulloblastoma we report underwent surgery followed by sequential radiotherapy and chemotherapy, resulting in a favorable prognosis. This may suggest that postoperative radiotherapy combined with chemotherapy could be effective in controlling adult medulloblastoma.