Background: Lung adenocarcinoma (LUAD) is a leading cause of mortality associated with cancer globally. Thus, it is essential to elucidate its tumorigenesis and prognosis. Accumulating evidence shows that long noncoding RNAs (lncRNAs) play important roles in the occurrence and progression of tumors by regulating their glucose metabolism.
Methods: Bioinformatics analysis was performed to explore the expression of in LUAD. The level of in LUAD cells and tissues was detected by RT-qPCR. CCK-8, colony formation, EDU and transwell assays were conducted to evaluate the cell growth and migration of LUAD cells (A549 and PC9). High throughput sequencing was used to discover the downstream genes of . The metabolic function of LUAD cells was identified by glucose uptake and lactate production assays. Furthermore, tumor xenografts were established to investigate the effects of on tumor growth in vivo.
Results: Herein, we found that was low-expressed in LUAD, and its level correlated with clinical prognosis. Ectopic expression of inhibited the proliferation and migration of LUAD cells (A549 and PC9). High throughput sequencing and gene enrichment analysis revealed that LINC0551 may be involved in metabolic pathway. Glucose uptake and lactate production assays suggested that suppressed glycolysis of LUAD cells. Mechanistically, our work revealed that inhibited glycolysis in LUAD cells by impairing -mediated transcription of an important glycolysis-related enzyme .
Conclusion: In summary, our study identifies as a tumor suppressor in LUAD and implicates the // axis in the glycolytic remodeling of LUAD.
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http://dx.doi.org/10.2147/OTT.S273797 | DOI Listing |
Oncol Res
January 2025
Department of Thoracic Surgery, The First Affiliated Hospital of Soochow University, Suzhou, 215006, China.
Background: Circular RNAs play an important role in regulating lung adenocarcinoma (LUAD). Bioinformatics analysis identified circ_0015278 as differentially expressed in LUAD. However, the biological mechanism of circ_0015278 in LUAD has not been fully clarified, especially in ferroptosis.
View Article and Find Full Text PDFClin Transl Med
February 2025
The Second Department of Thoracic Oncology, The Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University/Hunan Cancer Hospital, Changsha, Hunan Province, P.R. China.
To investigate the potential mechanisms underlying neutrophil extracellular traps (NETs) confer ferroptosis resistance and CD8(+) T cell inhibition in lung adenocarcinoma (LUAD). By the intravenous injection of LLC cells into the tail vein, a LUAD mouse model was created. Phorbol-12-myristate-13-acetate (PMA) stimulated neutrophils to facilitate NETs formation and combined with NETs inhibitor DNase I to explore NETs mechanism on LLC cell proliferation, migration, ferroptosis resistance, and CD8(+) T cell activity.
View Article and Find Full Text PDFImmunobiology
January 2025
Department of Pediatrics, Chinese and Western Medicine Hospital of Panzhihua, Panzhihua 617099, China.
Severe community-acquired pneumonia (SCAP) significantly threats the safety of children's lives. Long non-coding RNA (lncRNA) MANCR is overexpressed in lung adenocarcinoma (LUAD) tissue, promote the proliferation, invasion, and migration, decreased cell apoptosis of LUAD cells. This study aimed to detect lncRNA MANCR levels in pediatric SCAP, and explore the diagnostic and prognostic significance of MANCR in pediatric SCAP.
View Article and Find Full Text PDFBiomedicines
January 2025
Department of Immunology, The Fourth Military Medical University, Xi'an 710032, China.
The tumor microenvironment (TME) plays a crucial role in the progression of lung adenocarcinoma (LUAD). However, understanding its dynamic immune and stromal modulation remains a complex challenge. We utilized the ESTIMATE algorithm to evaluate the immune and stromal components of the LUAD TME from the TCGA database.
View Article and Find Full Text PDFThorac Cancer
January 2025
Department of Thoracic Surgery and Lung Transplantation, The Fifth Affiliated Hospital of Sun Yat-Sen University, Zhuhai, Guangdong, China.
Background: The mycobiome in the tumor microenvironment of non-smokers with early-stage lung adenocarcinoma (ES-LUAD) has been minimally investigated.
Methods: In this study, we conducted ultra-deep metagenomic and transcriptomic sequencing on 128 samples collected from 46 nonsmoking ES-LUAD patients and 41 healthy controls (HC), aiming to characterize the tumor-resident mycobiome and its interactions with the host.
Results: The results revealed that ES-LUAD patients exhibited fungal dysbiosis characterized by reduced species diversity and significant imbalances in specific fungal abundances.
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