Platelets are well-known for their functions in blood clotting and vascular repair. However, in recent years, the regulatory role of platelets in the occurrence and development of malignant tumors has received significant attention. While extensive research has been conducted on the regulation of tumors by circulating platelets in peripheral blood, there is a lack of coherence and continuity among these studies. The tumor microenvironment encompasses the intricate network of cellular and acellular elements that surround and interact with tumor cells, creating a supportive ecosystem for their survival and growth. It plays a crucial role in the initiation and progression of tumors. Similar to dark matter in the universe, platelets, as tiny and enigmatic entities, play an essential role in tumor development and treatment within the tumor microenvironment. Although our current understanding of platelet regulation in the tumor microenvironment is limited, they hold immense untapped potential. In-depth studies on the tumor microenvironment have revealed platelets as a meaningful component, influencing various aspects of tumor development, metastasis, and immune evasion. Platelets, through the release of various bioactive substances or direct interaction with tumor cells, impact tumor progression while being influenced by the tumor in return. Therefore, understanding the role and mechanisms of platelets in the tumor microenvironment is of great importance for tumor prevention and treatment. This review provides a summary of the research progress on the interplay between platelets and tumors in the tumor microenvironment, and presents a promising outlook on the potential of platelets in tumor therapy.

【Objective】 To explore the diagnostic value of platelet long non-coding RNA (lncRNA) as a biomarker for early screening of lung adenocarcinoma (LUAD). 【Methods】 The GSE183635 and GSE89843 datasets, which contained the platelet transcriptome of LUAD and healthy controls, were used for differential analysis, and the intersection of the differentially expressed lncRNA(DElncRNA) of the two datasets was taken. The expression levels of DElncRNA in LUAD tissues and normal control tissues were analyzed using GEPIA2. The expression levels of LINC01088 in platelets of 51 healthy controls and 54 LUAD patients were detected by quantitative Real-time PCR (qRT-PCR), and the diagnostic ability of each index was evaluated by ROC curve. 【Results】 8 DElncRNAs and 1 265 DElncRNAs were obtained from GSE183635 and GSE89843 datasets, respectively. The key DElncRNA LINC01088 was selected after intersection. GEPIA2 analysis showed that the expression level of LINC01088 in LUAD tissues was lower than that in normal lung tissues (P<0.05). Platelet LINC01088 was significantly downregulated in patients with LUAD and early-stage LUAD than in healthy controls(P<0.001). The area under the curve (AUC) of platelet LINC01088 in the diagnosis of LUAD was 0.755, the sensitivity was 81.1%, and the specificity was 67.9%. The AUC for early LUAD diagnosis was 0.727, the sensitivity was 80.0%, and the specificity was 67.9%. The AUC of the combined diagnostic model composed of platelet LINC01088 and carcinoembryonic antigen (CEA) for LUAD diagnosis was 0.807, the sensitivity was 89.2%, and the specificity was 71.4%. The AUC for early LUAD was 0.770, the sensitivity was 86.7%, and the specificity was 71.4%. The combined diagnostic model of platelet LINC01088 and CEA was superior to CEA in the diagnosis of LUAD and early LUAD (Z=-2.288, -2.34, both P<0.05). 【Conclusion】 LINC01088 is down-regulated in platelets of LUAD patients. Platelet LINC01088 may be a biomarker for early screening and diagnosis of LUAD.