microRNA-342-3p plays an important role in tumor occurrence and development. However, the expression pattern and roles of microRNA-342-3p in nonsmall cell lung cancer remain poorly understood. In the current study, we explored the roles and underlying mechanisms of microRNA-342-3p in nonsmall cell lung cancer via gain- and loss-of-function analyses. We used quantitative reverse-transcription-polymerase chain reaction and western blotting assays to measure the expression levels of microRNA-342-3p in nonsmall-cell lung cancer and B-cell lymphoma-2. Furthermore, we used small interfering RNA and RNA mimics to analyze the functions and underlying mechanisms of microRNA-342-3p in nonsmall cell lung cancer cells. A luciferase reporter assay was performed to evaluate the direct binding site of the 5'-untranslated region of B-cell lymphoma-2 targeted by microRNA-342-3p. We found that the expression of microRNA-342-3p was significantly lower in nonsmall cell lung cancer cells and tissues than in normal cells and tissues. The upregulation of microRNA-342-3p suppressed cell proliferation while promoting apoptosis in H1975, H460, and H226 cells. The overexpression of microRNA-342-3p in nonsmall cell lung cancer cells led to the downregulation of mRNA and protein levels in B-cell lymphoma-2 cells. Thus, B-cell lymphoma-2 was identified as a direct target of microRNA-342-3p. These findings indicate that microRNA-342-3p inhibits the growth of nonsmall cell lung cancer by repressing the expression of B-cell lymphoma-2, which suggests that microRNA-342-3p could be a potential target for the treatment of nonsmall cell lung cancer.
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http://dx.doi.org/10.1177/15330338211041193 | DOI Listing |
BMC Nurs
January 2025
Xiangya School of Nursing, Central South University, Changsha, China.
Background: A lung cancer diagnosis has a huge impact on the psychological well-being of both patients and family caregivers. However, the current psychological stress status among dyads remains unclear. We aimed to determine the prevalence of anxiety and depression and identify the factors that influence patients with lung cancer and their caregivers.
View Article and Find Full Text PDFBMC Cancer
January 2025
Department of Respiratory Medicine and Oncology, Yokohama Municipal Citizen's Hospital, 1-1, Mitsuzawa Nishimachi, Kanagawa Ku, Yokohama, 221-0855, Japan.
Introduction: The systemic immune-inflammation index (SII) has emerged as a promising prognostic marker in various malignancies. However, its prognostic significance in patients with small-cell lung cancer (SCLC) treated with immune checkpoint inhibitors (ICIs) remains unclear. In this study, we evaluated the prognostic impact of the SII in patients with SCLC after ICI use.
View Article and Find Full Text PDFPediatr Blood Cancer
January 2025
Pediatric Hematology and Oncology Department, University Hospital of Caen, Caen, France.
Background And Aims: Primary lung tumors (PLTs) in children are rare, and surgery remains the key to ensure remission. Here we describe the PLTs clinical characteristics, their management, and the pulmonary outcome following surgery.
Methods: We carried out a French national cohort of pediatric PLTs from 2013 to 2023 from the FRACTURE rare pediatric tumors national database.
Nat Rev Clin Oncol
January 2025
Department of Thoracic/Head and Neck Medical Oncology, the University of Texas, MD Anderson Cancer Center, Houston, TX, USA.
Immune-checkpoint inhibitors (ICIs) have transformed the treatment paradigm for advanced-stage squamous non-small-cell lung cancer (LUSC), a histological subtype associated with inferior outcomes compared with lung adenocarcinoma. However, only a subset of patients derive durable clinical benefit. In the first-line setting, multiple ICI regimens are available, including anti-PD-(L)1 antibodies as monotherapy, in combination with chemotherapy, or with an anti-CTLA4 antibody with or without chemotherapy.
View Article and Find Full Text PDFNPJ Precis Oncol
January 2025
Division of Experimental Chemotherapy, Cancer Chemotherapy Center, Japanese Foundation for Cancer Research, Tokyo, Japan.
KRAS-specific inhibitors have shown promising antitumor effects, especially in non-small cell lung cancer, but limited efficacy in colorectal cancer (CRC) patients. Recent studies have shown that EGFR-mediated adaptive feedback mediates primary resistance to KRAS inhibitors, but the other resistance mechanisms have not been identified. In this study, we investigated intrinsic resistance mechanisms to KRAS inhibitors using patient-derived CRC cells (CRC-PDCs).
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