B7-H3 (CD276) is an immune checkpoint from the B7 family of molecules and is abnormally expressed in tumor cells as a co-inhibitory molecule to promote tumor progression. Within the tumor microenvironment (TME), B7-H3 promotes tumor progression by impairing the T cell response, driving the polarization of tumor-associated macrophages (TAMs) to M2 phenotype, and inhibiting the function of other immune cells. In addition, B7-H3 promotes tumor cell proliferation, migration, invasion, metabolism disorder, angiogenesis, and resistance to treatment to promote tumor progression through its non-immunological functions. Immunotherapy targeting B7-H3, as well as combinations with other immune checkpoint therapies, have shown certain efficacy. In this review, we synthesizes the expression of B7-H3 and its mechanism to promote tumor progression through inducing immunomodulation and non-immunological functions, as well as its role of B7-H3 in tumor therapy, aiming to provide a reference for the clinical treatment of tumors.

The relationship between metabolism and cancer is a major focus of current research, with an increasing number of studies highlighting the significant role of various metabolites in tumor cells, such as lactate, acetic acid, lysine, serine, tryptophan, palmitic acid, succinate, etc. These metabolites are involved in numerous biological processes within tumor cells, including transcription, translation, post-translational modification (PTM) of proteins, cell cycle regulation, and metabolism, thereby modulating tumor proliferation, migration, and drug resistance. Metabolite-mediated PTMs of proteins undoubtedly play a vital role in tumor cells, affecting both histones and non-histone proteins, covering modifications such as lactylation, crotonylation, acetylation, palmitoylation, and succinylation. Therefore, this review aims to elaborate on the abnormal levels of some major metabolites, related metabolic pathways, and the latest protein acyl PTMs they mediate in tumor cells, providing new insights for diagnosis and therapy in the field of oncology.

Background: Transcriptional coactivator with PDZ-binding motif (TAZ) has been reported to be involved in tumor progression, angiogenesis, epithelial-mesenchymal transition (EMT), glycometabolic modulation and reactive oxygen species (ROS) buildup. Herein, the underlying molecular mechanisms of the TAZ-induced biological effects in bladder cancer were discovered. Methods: qRT-PCR, western blotting and immunohistochemistry were performed to determine the levels of TAZ in bladder cancer cells and tissues. CCK-8, colony formation, tube formation, wound healing and Transwell assays and flow cytometry were used to evaluate the biological functions of TAZ, miR-942-3p and growth arrest-specific 1 (GAS1). QRT-PCR and western blotting were used to determine the expression levels of related genes. Chromatin immunoprecipitation and a dual-luciferase reporter assay were performed to confirm the interaction between TAZ and miR-942. In vivo tumorigenesis and colorimetric glycolytic assays were also conducted. Results: We confirmed the upregulation and vital roles of TAZ in bladder cancer. TAZ-induced upregulation of miR-942-3p expression amplified upstream signaling by inhibiting the expression of large tumor suppressor 2 (LATS2, a TAZ inhibitor). MiR-942-3p attenuated the impacts on cell proliferation, angiogenesis, EMT, glycolysis and ROS levels induced by TAZ knockdown. Furthermore, miR-942-3p restrained the expression of GAS1 to modulate biological behaviors. Conclusion: Our study identified a novel positive feedback loop between TAZ and miR-942-3p that regulates biological functions in bladder cancer cells via GAS1 expression and illustrated that TAZ, miR-942-3p and GAS1 might be potential therapeutic targets for bladder cancer treatment.

PD-1 restrains effective killing of cancer cells by the immune system and is predominantly located on the surface of T cells or other immune cells. However, cancer cells also express PD-1 to varying degrees, which is commonly associated with a poor prognosis. Here, we investigated the regulation and function of PD-1 expression in prostate cancer (PCa) and revealed the impact on the tumor microenvironment. PD-1 expression in cancer cells positively correlated with Gleason grade and metastasis but negatively correlated with CD8+ T cell infiltration in PCa patients. PCa cells secreted PD-1 in exosomes that enhanced the activity of myeloid-derived suppressor cells (MDSCs) by activating JAK/STAT3 signaling. The activated MDSCs in turn reduced the infiltration of CD8+ T cells within the tumor, promoting tumor immune evasion. The ubiquitin-specific protease USP7 induced deubiquitination and elevated the abundance of PD-1 in PCa, and USP7 inhibition sensitized PCa tumors to anti-PD-1 antibody treatment. Given the modest efficacy of current immunotherapeutic approaches for PCa, strategies to inhibit the secretion of PD-1-bearing exosomes or USP7 function may emerge as promising immunostimulatory interventions for treating PCa.

Circular RNA (circRNA) is a newly discovered endogenous non-coding RNA (ncRNA), which is characterized with a closed circular structure. A growing body of evidence has verified the vital roles of circRNAs in human cancer. In this research, we selected circPPP1CB as a study object by circRNA sequencing and quantitative real-time PCR (qRT-PCR) validation in human bladder cancer (BC). CircPPP1CB is downregulated in BC and is negatively correlated with clinical stages and histological grades. Functionally, circPPP1CB modulated cell growth, metastasis, and epithelial-to-mesenchymal transition (EMT) process in vitro and in vivo. Mechanically, we performed various experiments to verify the circPPP1CB/miR-1307-3p/SMG1 regulatory axis. Taken together, our results demonstrated that circPPP1CB participates in tumor growth, metastasis, and EMT process by interacting with the miR-1307-3p/SMG1 axis, and that circPPP1CB might be a novel therapeutic target and diagnostic biomarker in human BC.

The present study aimed to investigate the potential mechanisms of human miR‑942 in the sunitinib‑resistance of renal cell carcinoma (RCC). A sunitinib‑resistant OS‑RC‑2 cell line was established by continuous exposure to increasing concentrations of sunitinib for ~12 weeks. The expression levels of four miRNAs were determined by reverse transcription‑quantitative (RT‑q)PCR. miR‑942 mimics were transfected into OS‑RC‑2 cells and RNA sequencing was performed on the miR‑942‑ and negative control‑transfected cells. Downregulated genes, including those of long non‑coding RNAs (lncRNAs) and mRNAs, were identified. The target genes of miR‑942 were predicted, followed by protein‑protein interaction network construction and functional enrichment analyses of miR‑942 target genes. In addition, RCC RNA‑seq and miRNA‑seq data were downloaded from The Cancer Genome Atlas (TCGA) database. The contributions of lncRNA and/or mRNAs to survival prediction were assessed and a competing endogenous RNA (ceRNA) network consisting of miR‑942, lncRNA and mRNAs was constructed. The expression levels of LINC00461, miR‑942, spalt‑like transcription factor 1 (SALL1), methionyl aminopeptidase 1 (METAP1) and DDB1 and CUL4 associated factor 1 (DCAF11) were verified using RT‑qPCR. The role of LINC00461 in cell viability was detected by MTT assay. The expression level of miR‑942 was significantly increased in sunitinib‑resistant cells. A total of seven lncRNAs and 155 mRNAs were predicted as target genes of miR‑942 in the miR‑942 mimic‑treated samples, compared with the mimic control‑treated group. These potential target genes were significantly associated with 'protein binding', 'TNF‑β signaling pathway', 'negative transcriptional regulation' and 'RNA binding'. Through the integrated analysis of RNA‑sequencing and TCGA data, an miR‑942‑related ceRNA network, which was predicted to significantly affect the survival of patients with RCC, was constructed. The expression levels of lncRNA LINC00461 and the genes SALL1, METAP1, and DCAF11 were further verified. The viability of OS‑RC‑2 cells was decreased following co‑transfection with miR‑942 mimics and LINC00641 siRNA, and was comparable to that of wild type OS‑RC‑2 cells (P>0.05). Therefore, lncRNA LINC00461 may act as an miR‑942 ceRNA, and affect the survival of patients with RCC by regulating the expression of SALL1, METAP1 and DCAF11.