Recent studies have shown that the innate immune cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING) pathway may play an important role in antitumor immunity. Additionally, the cGAS-STING pathway promotes the senescence of cancer cells, induces apoptosis of cancer cells, and increases the protective effect of cytotoxic T cells and natural killer cell-mediated cytotoxicity. We believe that the combination of the cGAS-STING signaling pathway with other therapeutic methods provides a new perspective from which to overcome obstacles in the application of this review. Further, we highlight the antitumor mechanism of the cGAS-STING signaling pathway and the latest advances in monotherapy and combination therapy with related agonists.

Background: The limitation of current biomarker of early stage ovarian cancer and the anatomical location of ovarian (depths of the pelvic) make ovarian cancer difficult to be detected in early stage. Growing evidence shows exosomes as key information transmitters, it carried molecules, such as miRNAs, proteins, lipids, double-stranded DNA have been reported as promising biomarkers in many diseases. However, little is known about the protein and lipid composition of ovarian cancer. Methods: Here, we report proteomic and lipidomic analysis of exosomes derived from ovarian cancer cells (SKOV-3) and ovarian surface epithelial cells (HOSEPiC). Results: A total of 1433 proteins and 1227 lipid species were identified from two cell line derived exosomes. Several lipid species and proteins significantly differ in SKOV-3 derived exosomes compared to those from HOSEPiC. For example, we noted that ChE and ZyE species were in general more abundant in exosomes from SKOV-3 than from HOSEPiC; Collagen type V alpha 2 chain (COL5A2) and lipoprotein lipase (LPL) were significantly higher in SKOV-3 derived exosomes than HOSEpic (p < 0.05). Conclusions: Our research indicates the promising role of exosomal proteins and lipids in the early diagnosis of ovarian cancer.

Exosomes are endosome-derived extracellular vesicles that are released upon the fusion of multivesicular bodies with the plasma membrane. These vesicles contain proteins, lipids, and nucleic acids and are found in various human body fluids. Exosomes can transfer bioactive molecules to nearby or distant recipient cells, thereby affecting their function. Recently, exosomes have gained importance as a medium of communication between tumor cells. An increasing number of studies have found that non-coding RNAs in tumor cell-derived exosomes can regulate tumor microenvironments, inhibit immune cell function, promote the growth and invasion of tumor cells, and impart resistance to chemicals in tumor cells. In this review, we focus on the effects of exosomal long non-coding RNAs (lncRNAs) on tumors. As exosomes and their parent cells have similar biological characteristics and coated lncRNAs can exist stably in vivo without being degraded by RNases, exosomal lncRNAs have emerged as novel non-invasive tumor biomarkers for use in the early diagnosis and evaluation of prognosis of tumors. Advancements in the field have led to the development of a variety of techniques in exosomal non-coding RNA research. Currently, most methods include the separation and purification of exosomes, followed by RNA extraction, reverse transcription, and subsequent analyses; thus, these processes are very tedious and vulnerable to contamination and could lead to inaccurate and inconsistent results. Thus, there has been an increase in the development of detection methods for exosomal RNAs. Here, we discuss the existing research methods, their advantages and disadvantages, and a few new techniques.

Due to the success of chimeric antigen receptors (CARs) in hematological tumors, CARs are also being studied to treat solid tumors. Improving the ability of CARs to penetrate solid tumor tissues is one of the biggest challenges. As the most malignant cancer of the female reproductive system, the survival rate of ovarian cancer has not been significantly improved by traditional therapy methods; therefore, it is necessary to develop new therapeutic targets and new immunotherapy methods for ovarian cancer. UPAR is a glysocylphosphatidylinositol (GPI) anchoring membrane protein that is differentially expressed in normal tissues and ovarian cancer tissues. It has been shown that uPAR up-regulation promotes tumor development, proliferation, invasion, and metastasis, and uPAR is also up-regulated in tumor matrix components. In our study, CARs were designed using the natural ligand binding fragment of uPAR for ovarian cancer.

Background. Cervical squamous cell carcinoma (CSCC) is the main pathological type of cervical cancer, accounting for 80%–85% of cervical cancer. Owing to concurrent chemoradiotherapy (CCRT) resistance in a subset of CSCC patients, the treatment response is often unsatisfactory. Identifying predictors and therapeutic targets related to cisplatin‐based CCRT resistance in CSCC is critical. Methods. We reanalyzed GSE56363, an mRNA dataset from the GEO database with 21 patients with locally advanced CSCC, to identify differentially expressed genes (DEGs) related to CCRT resistance. The hub genes were screened from the protein‐protein interaction network of DEGs using cytoHubba plug‐in of Cytoscape software. Transcriptome sequencing technology was used to compare differential expression between SiHa cells overexpressing BRCA1 compared with control SiHa cells. Functional annotation for DEGs and gene set enrichment analysis (GSEA) was performed to identify DEG‐enriched relative signaling pathways to examine the molecular mechanisms of BRCA1 in CCRT resistance of CSCC. qPCR was used to verify the expression of key genes in SiHa/DDP cells. Results. A total of 609 DEGs including 223 upregulated DEGs and 386 downregulated DEGs were identified between the complete response to CCRT (CR) and noncomplete response to CCRT (NCR) CSCC patients based on the GSE56363 dataset. Ten hub genes with the highest degrees were identified via the plug‐in CytoHubba in Cytoscape: BRCA1, CDCA8, ASPM, CDC45, RAD51, HMMR, CENPF, EXO1, DTL, and ZWINT genes, and BRCA1 ranked first. Through transcriptome sequencing analysis based on GSE141558, 1344 DEGs were identified in BRCA1‐overexpressing SiHa cells, including 824 upregulated DEGs and 520 downregulated DEGs. GSEA results showed that CCRT‐resistance related signaling pathways, such as the JAK/STAT signaling pathway and the WNT signaling pathway, were differentially enriched in BRCA1‐expressing SiHa cells. STAT1, STAT2, and CCND1 were screened as the differentially expressed target genes of BRCA1 and may correlate with resistance of CSCC. qPCR results showed that only STAT1 was significantly increased in SiHa cells with GV230‐BRCA1 plasmid transfection. Conclusion. BRCA1 overexpression in SiHa cells may upregulate STAT1 to activate the JAK/STAT signaling pathway, suggesting a mechanism for enhanced CCRT resistance.