Background: Acyl‐coenzyme A cholesterol acyltransferase (ACAT) is a membrane‐binding enzyme localized in the endoplasmic reticulum. ACAT2 can promote the development of colon cancer, but its efficacy in lung adenocarcinoma (LUAD) remains uncertain.Method: ACAT2 expression was performed by using the TIMER2.0 database. The GEPIA database was utilized to analyze the correlation between ACAT2 expression and pathological stage of the tumor. Clinical prognosis was assessed through the Kaplan–Meier analysis. The CancerSEA database was employed to scrutinize the correlations between the ACAT2 expression and the functional status of various tumors, which were subsequently visualized as a heatmap. Furthermore, molecular interaction network analysis was performed by the STRING tool.Results: High ACAT2 expression was associated with a poor DFS and OS in LUAD patients. Cox regression analysis indicated that the poor outcomes may be related to tumor stage, nodal stage, distant metastatic stage. ACAT2 was found to play a crucial role in various biological processes, including the cell cycle, DNA repair, DNA damage response, and proliferation. Enrichment pathway analysis revealed four ACAT2 related genes, ACOX1, EHHADH, OXCT1, and DLAT.Conclusion: Our study showed that ACAT2 was upregulated in LUAD, and had a worse survival. ACAT2 could be a novel predictive biomarker and therapeutic target in LUAD.

NLRC3, a negative regulator, exhibits considerable potential in the realm of lung cancer immunotherapy by virtue of its profound impact on the immune response intensity, primarily through its regulatory effects on the cGAS-STING pathway. The inhibition of NLRC3 has been found to augment the activity of the aforementioned pathway, thereby enhancing the anti-tumor immune response. This comprehensive review endeavors to elucidate the molecular and genetic structures of NLRC3, its role within the immune system, and its interaction with the cGAS-STING pathway, with a particular emphasis on its potential applications in lung cancer immunotherapy. Existing research underscores NLRC3's capacity to mitigate excessive immune responses via the negative regulation of the cGAS-STING pathway, thus underscoring its significant regulatory role in lung cancer immunotherapy. The development of pharmaceutical interventions and gene therapy strategies targeting NLRC3 presents a promising avenue for the creation of novel therapeutic options for individuals afflicted with lung cancer. Nonetheless, the clinical application of these therapies is confronted with both technical and biological challenges. This review aims to provide a theoretical foundation for related research endeavors and delineate future research directions in this field.

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Succinylation has been shown to promote lung cancer development, but its mechanism remains incompletely understood. KAT2A, a succinyltransferase, acts as an oncogene in multiple cancers, but its role in mediating lung cancer progression is unclear. This study aimed to investigate the mechanism by which KAT2A regulates lung cancer progression via succinylation. KAT2A expression was analyzed using UALCAN, GEPIA, and Kaplan–Meier Plotter databases, and validated in lung cancer cell lines and patient‐derived tissues. Quantitative real‐time PCR, Cell Counting Kit‐8 (CCK‐8), EdU staining, and flow cytometry were performed to assess KAT2A's role in lung cancer cell proliferation and apoptosis. KAT2A's target proteins were predicted using LinkedOmics and STRING databases. Additionally, in vivo xenograft models were established to evaluate the effect of KAT2A knockdown on tumor growth. Results indicated that KAT2A expression was significantly elevated in lung cancer cells and tissues and was associated with poor prognosis. KAT2A knockdown inhibited proliferation and promoted apoptosis in lung cancer cells, whereas MYC overexpression reversed these effects. Mechanistically, KAT2A knockdown downregulated MYC by reducing succinylation at K370 and K386 residues. Mutation of these sites abrogated the proliferative effect of MYC overexpression and restored apoptotic activity. Furthermore, in vivo experiments demonstrated that KAT2A knockdown inhibited tumor growth and reduced MYC succinylation. Our findings demonstrate that KAT2A functions as an oncogene in lung cancer by enhancing MYC succinylation. This study identifies KAT2A as a promising therapeutic target for lung cancer.

肺癌脑膜转移病死率极高。循环肿瘤DNA（circulating tumor DNA, ctDNA）已被证实含有肿瘤的基因组改变信息，并已被用于监测肿瘤的进展和对治疗的响应。对于存在脑膜转移瘤的患者，由于血脑屏障等因素的存在，外周血ctDNA不能反映脑部病灶的信息，此时脑脊液ctDNA作为检测样本能更好地体现颅内肿瘤的基因状态，指导临床对颅内病灶的靶向治疗。本研究旨在探究脑脊液ctNDA用于监测非小细胞肺癌（non-small cell lung cancer, NSCLC）脑膜转移的可行性以及脑脊液ctDNA检测对NSCLC脑膜转移的临床价值。 入组NSCLC脑膜转移患者21例，通过二代基因测序技术对患者的脑脊液及外周血样本进行基因检测，并进行脑脊液细胞学病理学检测和头颅核磁共振增强检查。 入组21例患者脑脊液中均检测到ctDNA。脑脊液ctDNA检测的灵敏性在脑膜转移诊断方面优于细胞学（P < 0.001）。脑脊液的基因突变检出率及基因突变丰度均高于血浆（P < 0.001）。脑脊液具有独特的基因谱。6例动态检测的患者中，脑脊液中ctDNA丰度变化均同时或早于临床疾病变化出现，可及时揭示耐药机制和监测复发趋势。 脑脊液ctDNA检出率高于细胞学及影像学；脑脊液ctDNA检测可展现脑膜转移病灶特有的突变图谱；脑脊液ctDNA动态监测对肺癌患者临床疗效具有提示意义。