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Background: The crucial roles played by lncRNA-AC068228.1 in primary malignant cancer remain poorly understood. This study aimed at examining the clinical significance and evaluating the biological function of AC068228.1 in lung adenocarcinoma (LUAD).
Methods: We used data obtained from The Cancer Genome Atlas (TCGA), Genotype-Tissue Expression (GTEx), and the Gene Expression Omnibus (GEO) database to examine the expression of AC068228.1 in LUAD patients, and the prognostic and diagnostic value of those levels. Functional experiments were conducted to determine the function of AC068228.1 on LUAD cells. Signaling pathway enrichment analysis of AC068228.1 was conducted using the clusterProfiler and Gene Set Enrichment Analysis (GSEA) software. We analyzed the correlation between AC068228.1 expression and immune infiltration level in LUAD using the single-sample gene set enrichment analysis (ssGSEA) method by the R package GSVA.
Results: AC068228.1 expression was significantly elevated in LUAD tissues compared with normal tissues. Higher expression of AC068228.1 was strongly correlated with adverse clinical outcomes and was identified as an independent prognostic marker for LUAD patients. GSEA and infiltration analysis confirmed that AC068228.1 expression was significantly correlated with immune cells infiltrating in LUAD. Knockdown of AC068228.1 inhibited the cell proliferation and cell migration of LUAD.
Conclusions: AC068228.1 was upregulated in LUAD and was significantly correlated with adverse clinical outcomes. Meanwhile, it was associated with immune cell infiltration and could be used as a promising diagnostic and prognostic biomarker for LUAD patients.
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http://dx.doi.org/10.3389/fonc.2022.856655 | DOI Listing |
Br J Cancer
September 2025
Department of Genetics, Institut Curie, PSL Research University, Paris, France.
Background: Identifying molecular alterations specific to advanced lung adenocarcinomas could provide insights into tumour progression and dissemination mechanisms.
Method: We analysed tumour samples, either from locoregional lesions or distant metastases, from patients with advanced lung adenocarcinoma from the SAFIR02-Lung trial by targeted sequencing of 45 cancer genes and comparative genomic hybridisation array and compared them to early tumours samples from The Cancer Genome Atlas.
Results: Differences in copy-number alterations frequencies suggest the involvement in tumour progression of LAMB3, TNN/KIAA0040/TNR, KRAS, DAB2, MYC, EPHA3 and VIPR2, and in metastatic dissemination of AREG, ZNF503, PAX8, MMP13, JAM3, and MTURN.
J Thorac Oncol
September 2025
Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Seoul National University Bundang Hospital, Seongnam, Republic of Korea; Emeritus Professor, Seoul National University College of Medicine, Seoul, Republic of Korea.
Introduction: Multifocal subsolid nodules (SSNs) are increasingly detected with widespread lung cancer screening and advanced thoracic imaging, representing a spectrum of multifocal lung adenocarcinomas (LUADs). When synchronous SSNs coexist with a surgically confirmed subsolid LUAD, their trajectories remain poorly understood, contributing to uncertainty regarding optimal management strategies. This study aimed to evaluate the clinical course and impact of synchronous SSNs in such patients and to identify features associated with their progression.
View Article and Find Full Text PDFGenes Genomics
September 2025
Department of Clinical Laboratory, The First Affiliated Hospital of Guilin Medical University, Le Qun Road 15, Guilin, 541001, Guangxi, China.
Background: Lung cancer (LC) is the leading cause of cancer-related deaths globally. Genetic variants in mismatch repair (MMR) genes, such as MutS homolog 2 (MSH2), MutS homolog 6 (MSH6) and MutL homolog 1 (MLH1), may influence individual susceptibility and clinical outcomes in LC.
Objective: This study investigated the associations of genetic polymorphisms in MSH2, MSH6, and MLH1 with susceptibility and survival outcomes in lung cancer patients in the Guangxi Zhuang population.
Mol Cell Biochem
September 2025
Department of Laboratory Medicine, The People's Hospital of Zhongjiang, No. 96, Dabei Street, Kaijiang Town, Zhongjiang County, Deyang City, 618100, Sichuan Province, China.
5-methylcytosine (m5C) methylation is a post-transcriptional modification of RNAs, and its dysregulation plays pro-tumorigenic roles in lung adenocarcinoma (LUAD). Here, this study elucidated the mechanism of action of NSUN2, a major m5C methyltransferase, on LUAD progression. mRNA expression was analyzed by quantitative PCR.
View Article and Find Full Text PDFInt J Surg
September 2025
Department of Respiratory and Critical Care Medicine, Hubei Province Clinical Research Center for Major Respiratory Diseases, Key Laboratory of Pulmonary Diseases of National Health Commission, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China
Background: Precise preoperative discrimination of invasive lung adenocarcinoma (IA) from preinvasive lesions (adenocarcinoma in situ [AIS]/minimally invasive adenocarcinoma [MIA]) and prediction of high-risk histopathological features are critical for optimizing resection strategies in early-stage lung adenocarcinoma (LUAD).
Methods: In this multicenter study, 813 LUAD patients (tumors ≤3 cm) formed the training cohort. A total of 1,709 radiomic features were extracted from the PET/CT images.