Role of long non-coding RNA ELFN1-AS1 in carcinogenesis.

As one of the leading causes of death worldwide, cancer significantly burdens patients and the healthcare system. The role of long non-protein coding RNAs (lncRNAs) in carcinogenesis has been extensively studied. The lncRNA ELFN1-AS1 was discovered recently, and subsequent studies have revealed its aberrantly high expression in various cancer tissues. In vitro and in vivo experiments have consistently demonstrated the close association between increased ELFN1-AS1 expression and malignant tumor characteristics, particularly in gastrointestinal malignancies. Functional assays have further revealed the mechanistic role of ELFN1-AS1 as a competitive endogenous RNA for microRNAs, inducing tumor growth, invasive features, and drug resistance. Additionally, the investigation into the clinical implication of ELFN1-AS1 has demonstrated its potential as a diagnostic, therapeutic, and, notably, prognostic marker. This review provides a comprehensive summary of evidence regarding the involvement of ELFN1-AS1 in cancer initiation and development, highlighting its clinical significance.

Unveiling the potential of FOXO3 in lung cancer: From molecular insights to therapeutic prospects.

Lung cancer poses a significant challenge regarding molecular heterogeneity, as it encompasses a wide range of molecular alterations and cancer-related pathways. Recent discoveries made it feasible to thoroughly investigate the molecular mechanisms underlying lung cancer, giving rise to the possibility of novel therapeutic strategies relying on molecularly targeted drugs. In this context, forkhead box O3 (FOXO3), a member of forkhead transcription factors, has emerged as a crucial protein commonly dysregulated in cancer cells. The regulation of the FOXO3 in reacting to external stimuli plays a key role in maintaining cellular homeostasis as a component of the molecular machinery that determines whether cells will survive or dies. Indeed, various extrinsic cues regulate FOXO3, affecting its subcellular location and transcriptional activity. These regulations are mediated by diverse signaling pathways, non-coding RNAs (ncRNAs), and protein interactions that eventually drive post-transcriptional modification of FOXO3. Nevertheless, while it is no doubt that FOXO3 is implicated in numerous aspects of lung cancer, it is unclear whether they act as tumor suppressors, promotors, or both based on the situation. However, FOXO3 serves as an intriguing possible target in lung cancer therapeutics while widely used anti-cancer chemo drugs can regulate it. In this review, we describe a summary of recent findings on molecular mechanisms of FOXO3 to clarify that targeting its activity might hold promise in lung cancer treatment.

Thymoquinone reversed doxorubicin resistance in U87 glioblastoma cells via targeting PI3K/Akt/mTOR signaling.

Natural compounds such as thymoquinone (TQ) have recently gained increasing attention in treating glioblastoma (GBM). However, the effects of TQ in reversing drug resistance are not completely understood. Therefore, we aimed to examine TQ impacts on GBM cells with doxorubicin (DOX) resistance and the involvement of the PI3K/Akt/mTOR pathway. GBM cancer U87 and U87/DOX (resistant cells) cells were exposed to DOX and TQ, and cell proliferation was assessed by the MTT assay. ELISA was applied to evaluate cell apoptosis. The expression of apoptotic mediators such as Caspase-3, Bax, Bcl-2 and PI3K, Akt, mTOR, P-gp, and PTEN was assessed via qRT-PCR and western blot. We found that a combination of TQ and DOX suppressed dose-dependent cell growth capacity in cells and increased the cytotoxic effects of DOX in resistant cells. In addition, TQ treatment increased DOX-mediated apoptosis in U87/DOX cell lines via modulating the pro- and anti-apoptotic markers. A combination of TQ and DOX upregulated PTEN and downregulated PI3K, Akt, and mTOR, suppressing this signal transduction in resistant cells. In conclusion, we showed TQ potentiated doxorubicin-mediated antiproliferative and pro apoptotic function DOX-resistant glioblastoma cells, which is mediated by targeting and suppressing PI3K/Akt/mTOR signal transduction.

Prognostic value of CT scan-based radiomics in intracerebral hemorrhage patients: A systematic review and meta-analysis.

OBJECTIVES: We conducted a systematic review and meta-analysis of current publications on the potential role of non-contrast-enhanced computed tomography (NCCT) radiomics as a prognostic indicator in patients with intracerebral hemorrhage (ICH). METHODS: We systematically searched PubMed, EMBASE, and the Web of Science from inception until January 8, 2024. Studies with NCCT-based radiomics features for predicting the prognostic outcomes of ICH patients were included. We calculated the pooled sensitivity, specificity, diagnostic odds ratio (DOR), and area under curve (AUC) values. The radiomics quality score (RQS), METhodological RadiomICs Score (METRICS), and the quality assessment of diagnostic accuracy studies (QUADAS-2) were used for quality assessment. RESULTS: Twenty-two studies were included. The pooled sensitivity, specificity, DOR, and AUC of radiomics models were 0.73, 0.78, 10.03, and 0.83, respectively, while on the combined radiomics models with other non-radiomics features were 0.80, 0.80, 16.28, and 0.86. Subgroup analysis showed that studies with the following covariates have a higher accuracy: single center, modified Rankin Scale (mRS) criteria for the ICH outcomes assessment, following patients for evaluation of ICH outcomes for more than a month, automatic segmentation, capturing the radiomics feature from the only intra-hematomal region, using PyRadiomic tool for features extraction, and using non-logistic regression for modeling. The quality of literature using QUADAS-2 and METRICS tools was good and was under-average using the RQS tool. No publication bias was detected. CONCLUSIONS: Radiomics features showed moderate to high accuracy for predicting ICH prognostic outcomes. Although the QUADAS-2 and METRICS assessments indicated good quality, the radiomics pipeline quality was under-average. CLINICAL RELEVANCE: NCCT-based radiomics features can provide information about the prognostic outcomes of ICH patients after patient admission. This study exploits the value of current evidence on NCCT-based radiomics methodology in the prediction of ICH prognosis.

Current approaches in glioblastoma multiforme immunotherapy.

Glioblastoma multiform (GBM) is the most prevalent CNS (central nervous system) tumor in adults, with an average survival length shorter than 2 years and rare metastasis to organs other than CNS. Despite extensive attempts at surgical resecting, the inherently permeable nature of this disease has rendered relapse nearly unavoidable. Thus, immunotherapy is a feasible alternative, as stimulated immune cells can enter into the remote and inaccessible tumor cells. Immunotherapy has revolutionized patient upshots in various malignancies and might introduce different effective ways for GBM patients. Currently, researchers are exploring various immunotherapeutic strategies in patients with GBM to target both the innate and acquired immune responses. These approaches include reprogrammed tumor-associated macrophages, the use of specific antibodies to inhibit tumor progression and metastasis, modifying tumor-associated macrophages with antibodies, vaccines that utilize tumor-specific dendritic cells to activate anti-tumor T cells, immune checkpoint inhibitors, and enhanced T cells that function against tumor cells. Despite these findings, there is still room for improving the response faults of the many currently tested immunotherapies. This study aims to review the currently used immunotherapy approaches with their molecular mechanisms and clinical application in GBM.