Cancer, a global health menace, continues to pose significant challenges in terms of incidence and mortality, necessitating innovative therapeutic strategies. Despite existing treatments, the limitations persist, prompting a quest for novel approaches. The emergence of immunotherapy marked a transformative era in solid tumor treatments, yet its efficacy is constrained by adverse effects. Concurrently, the integration of advanced technologies into cancer treatment explores the vast potential residing at the molecular level through gene analysis and manipulation. This review articulates the role of state-of-the-art genome editing technology, notably clustered regularly interspaced short palindromic repeats (CRISPR-Cas9), in overcoming the constraints of immunotherapy for cancers. Unveiling the intricacies of CRISPR-Cas9-mediated genome editing, the review introduces the formidable CRISPR toolbox. A spotlight is cast on the transformative impact of CRISPR-induced double-strand breaks (DSBs) on cancer immunotherapy, encompassing knockout and knock-in strategies. The utilization of CRISPR/Cas9 technology in pre-clinical cancer research has demonstrated notable success; however, its transition to the clinical setting remains in the nascent stages of development. This review aims to elucidate the fundamental aspects of CRISPR technology and offer a comprehensive survey of its existing applications while outlining its prospective role in the realm of cancer therapies. Through an exploration of CRISPR's mechanisms, current applications, and anticipated future potentials, this review provides valuable insights into the evolving landscape of CRISPR-based cancer treatment strategies.

Nanomaterials have shown great potential in anti-tumor applications and are currently the focus of research. This review article aims to provide a comprehensive overview of the challenges encountered in oncology treatment and how nanomaterials are being utilized to overcome these obstacles. The authors discuss the limitations of conventional treatments, including limited efficacy, side effects, and toxicity issues. They highlight the importance of early tumour diagnosis and personalized treatment plans, as well as the need for innovative therapeutic approaches such as targeted therapy, immunotherapy, and gene therapy. The article primarily focuses on how nanomaterials can be engineered to achieve specific recognition and aggregation within tumour tissues through surface modifications involving targeting molecules such as antibodies, peptides, and receptor ligands. This surface modification technique facilitates improved targeting in the targeting of photodynamic therapy, while minimizing harm to normal tissues. The authors also discuss the potential and future prospects of nanomaterials in tumour therapy, including breakthroughs in their application, biosafety concerns, biocompatibility issues, preparation processes, clinical translation challenges, interdisciplinary cooperation, international exchange, relevant regulations and ethical guidelines. Overall, this review highlights the substantial potential of nanomaterials in oncology treatment, emphasizing the need for careful consideration of safety concerns to ensure their safe and effective application. The authors conclude that strengthening interdisciplinary cooperation and international exchange will contribute to the healthy development of nanomaterials in oncology treatment.

The latent transforming growth factor-beta (TGF-β) binding protein 1 (LTBP1) has been implicated in various cellular processes, but its role in triple-negative breast cancer (TNBC) remains unclear. In this study, we investigated the impact of LTBP1 on TNBC progression and its underlying mechanisms. Analysis of online datasets revealed elevated LTBP1 mRNA expression in breast cancer tissues compared to normal adjacent tissues. Kaplan-Meier Plotter analysis indicated that high LTBP1 expression was negatively correlated with relapse-free survival (RFS), distant-metastasis free survival (DMFS), and overall survival (OS) of breast cancer patients. Additionally, LTBP1 mRNA levels were associated with chemotherapy resistance. Functional assays in TNBC cells demonstrated that LTBP1 knockdown suppressed cell proliferation, induced apoptosis, and attenuated migration and invasion. In vivo studies confirmed that LTBP1 knockdown inhibited tumor growth in a xenograft mouse model. Mechanistically, LTBP1 positively correlated with genes involved in signaling regulation and organelle organization, with significant associations to GTPase binding and the RhoA/ROCK pathway. LTBP1 knockdown reduced RhoA activity and phosphorylation of Myosin Light Chain 2 (MLC2), suggesting inhibition of the RhoA/ROCK signaling pathway. Moreover, activation of the RhoA/ROCK pathway partially rescued the effects of LTBP1 knockdown on TNBC cell proliferation, apoptosis, migration, and invasion. In conclusion, our findings suggest that LTBP1 promotes TNBC progression through activation of the RhoA/ROCK signaling pathway, highlighting its potential as a therapeutic target for TNBC.

Background: Bladder cancer (BLCA), particularly invasive BLCA, has become a medical burden worldwide as it is associated with recurrence and easy metastasis. There are specific differences in the expression of various miRNAs in tumor and normal tissues. Hence, miRNAs can be used as biomarkers for tumor diagnosis and prognostic evaluation. The current study aimed to predict the downstream target genes of BLCA-related miRNAs and explore their association with immune infiltration. Method: Data on BLCA-related mRNA and miRNA expression levels were downloaded from The Cancer Genome Atlas. Correlation analysis and Cox regression analysis were performed to validate the miRNA risk model. The infiltration of various immune cells should be compared to determine the distinct differences between the immunological microenvironment of the two risk groups. Results: A predictive framework of BLCA was established using the expression levels of two miRNAs. Cox regression analysis showed that the low-risk group had a better prognosis. Then, the target genes of miRNA were predicted, and the target genes were analyzed using Gene Ontology and Kyoto Encyclopedia of Genes and Genomes. Moreover, variations in immune cells and functions between the high- and low-risk groups were assessed. Conclusion: The prognostic features composed of two associated miRNAs (MIR-25, MIR-548AN) may help predict the overall survival of BLCA.

Objective: The DSS was utilized to construct colitis model of mouse. The colitis mice were colonized with gut microbiota. The effects of gut microbial metabolites on colitis were studied. The mechanisms of gut microbial metabolites to improve intestinal immunity were also further explored. Methods: The male BALB/c mice were selected to construct colitis mouse model with DSS and colonized with gut microbiota. The content of short-chain fatty acids in intestinal metabolites of mice during modeling were detected with GC-MS. After the mice were sacrificed, the colon tissue was stained to observe the colitis in different groups of mice. The contents of IL-22 and IL-17 in colon tissue was determined with ELISA method. To study the mechanism of relieving colitis, qRT-PCR and western blotting were used to study the horizontal of Ffar2 gene and pSTAT3 and pAKT in colon tissue, respectively. The congenital lymphocytes were isolated and purified, and the migration ability of the congenital lymphocytes was examined by cell scratch plane migration test. Results: The colonization of the gut microbiota had significant effects on the contents of short-chain fatty acids in the intestinal metabolites of colitis mice, of which the effect on the content of acetic acid and butyric acid was more significant. The colonization of gut microbiota could effectively relieve colitis in mice and effectively promote the secretion of IL-22 in colon tissue. Studying the remission mechanism indicated that colonization of gut microbiota with colitis could effectively promote the expression of Ffar2 gene in colon tissue and increase the expression of pSTAT3 and pAKT protein. The migration ability of the lymphocyte was significantly upregulated in the model group compared with the other groups, demonstrating that DSS can effectively activate the lymphocyte; The migration of congenital lymphocyte in the experimental group was significantly alleviated than that in the model group, but it was up-regulated than that in the positive control group, and the colonic tissue of the positive control group was similar to that of the normal group. Conclusion: The short-chain fatty acids in the intestinal flora metabolites can promote the gene expression of the metabolite-sensitive receptor Ffar2. The effective combination of short-chain fatty acids and Ffar2 receptors can promote the phosphorylation of STAT3 and AKT proteins, effectively promote the secretion of IL-22 in intestinal ILC3 cells, alleviate colitis in mice, and thereby improve their intestinal immune function.

Metastasis is the major cause of cancer-related mortality. Metastasis is a process through which cancer spreads from its initial location to other sections of the body. Cancer cells' epithelial-mesenchymal transition (EMT), anoikis resistance, cell migration, and angiogenesis are all well-known steps in this process. Investigating the molecular processes that govern cancer metastatic progression may lead to more effective diagnostic and treatment strategies. Long non-coding RNAs (lncRNAs) have recently discovered to have a vital more than 200 nucleotides. A rising body of research indicates that lncRNAs have a role in a wide range of biological processes and diseases, including cancer. The usage of LncRNA in cancer metastasis has been widely researched. However, according to current studies, lncRNA is mostly associated with the EMT process. This review focuses on the processes behind lncRNA involvement in cancer metastasis.

Adenosine alterations to RNA, which are largely determined by RNA modification writers (RMWs), are critical for cancer growth and progression. These RMWs can catalyze different types of adenosine modifications, such as N6-methyladenosine (m6A), N1-methyladenosine (m1A), alternative polyadenylation (APA), and adenosine-to-inosine (A-to-I) RNA editing. These modifications have profound effects on gene expression and function, such as immune response, cell development. Despite this, the clinical effects of RMW interactive genes on these cancers remain largely unclear. A comprehensive analysis of the clinical impact of these epigenetic regulators in pan-cancer requires further comprehensive exploration. Here, we systematically profiled the molecular and clinical characteristics of 26 RMWs across 33 cancer types using multi-omics datasets and validated the expression level of some RMWs in various cancer lines. Our findings indicated that a majority of RMWs exhibited high expression in diverse cancer types, and this expression was found to be significantly associated with poor patient outcomes. In the genetic alterations, the amplification and mutation of RMWs were the dominant alteration events. Consequently, the RNA Modification Writer Score (RMW score) was established as a means to assess the risk of RMWs in pan-cancer. We found that 27 of 33 cancers had significantly higher scores compared with normal tissues, and it was significantly correlated with prognosis. We also evaluated their impact on the tumor microenvironment and the response to immunotherapy and targeted therapy. These findings verified the important role of RMWs in different aspects of cancer biology, and provided biomarkers and personalized therapeutic targets for cancer.

Transition metal sulfides/transition metal phosphides (TMS/TMP) has shown great potential in cancer diagnosis and treatment due to its unique structural, optical, acoustic and magnetic properties. TMS/TMP can be formed from sulfur/phosphorus source and metal into binary compounds, or from the interaction of hydrogen sulfide (or hydrogen sulfuric acid) with metal oxides or hydroxides. It has a series of unique properties, such as high conductivity, metalloid properties, a variety of valence states and adjustable structure and so on. These advantages make it have great potential in biomedical applications, such as diagnostic imaging, disease therapy and drug/gene delivery. This review presents the latest research progress of TMS/TMP on tumor imaging, diagnosis and treatment. Here, we first illustrate the synthesis approaches and surface modification of TMS/TMP. Then, its emerging applications in tumor diagnosis and therapy are highlighted. Moreover, the challenges of TMS/TMP-mediated diagnosis/treat are provided and the prospective for this field are discussed.

As a reversible post-transcriptional modification, N6-methyladeno sine is the most common form of RNA modification in eukaryotic mRNA. Cancer stem cells (CSCs), which are a subpopulation of cells with self-renewal ability and differentiation potential, have been regarded to be one of the roots of tumor occurrence, recurrence, and metastasis. Currently, numerous studies have demonstrated that m6A RNA modification is critically implicated in the regulation of CSCs stemness or the CSC-like traits of cancer cells. This review summarized the effects of m6A RNA modification-related enzymes and underlying mechanisms contributing to CSCs or cancer cell stemness, which may provide novel targets and research directions for the specifical elimination of CSCs or cancer cells with stemness.

Ferroptosis, a recently identified form of programmed cell death, is characterized by the accumulation of lipid peroxidation, reactive oxygen species, and elevated free iron levels, involving the regulation of glutathione metabolism, iron metabolism, lipid metabolism, and oxidative stress biology. Tumor metastasis, a critical hallmark of malignancy and a key contributor to cancer recurrence and mortality, has been extensively linked to iron dysregulation, highlighting the potential of agents inducing iron-mediated cell death as promising strategies for preventing and treating metastasis. This review offers a comprehensive understanding the regulatory mechanisms underlying ferroptosis and its crucial role in the three distinct stages of metastasis: invasion, circulation, and colonization.

Metadherin (MTDH), also known as LYRIC or AEG-1, is an oncogene that enhances tumor progression, metastasis, drug resistance, and immune escape in various cancers by modulating multiple oncogenic pathways, including NF-κB, PI3K/AKT, Wnt/β-catenin, MAPK, and AMPK. Due to the unknown of the complete structure of MTDH, the deep mechanisms of MTDH and selective inhibitors targeting MTDH remain to be explored. The Protein-Protein interaction (PPI) with the Staphylococcal nuclease domain containing 1 (SND1) is a crucial mechanism underlying the function of MTDH. Current studies have demonstrated that inhibitors, including antisense oligonucleotides, peptides, and small molecules targeting MTDH or MTDH-SND1 interactions, provide novel strategies to inhibit the oncogenetic effects of MTDH. This review summarizes and discusses the structure, function, and regulation of MTDH in cancers, providing the potential therapeutic perspectives of MTDH or MTDH-SND1 PPI for drug discovery.

Background: Hepatocellular carcinoma (HCC) stands out as one of the most lethal cancers globally, given its complexity, recurrence following surgical resection, metastatic potential, and inherent heterogeneity. In recent years, researchers have systematically elucidated the significance of long non-coding RNA (lncRNA) in the initiation and progression of HCC. The introduction of The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases has significantly enhanced the prognostic assessment of HCC. However, the association between HCC and cell senescence has been infrequently explored in the literature. Method: We downloaded liver hepatocellular carcinoma (LIHC)-related messenger RNA and lncRNA expression levels from TCGA. Correlation analysis, Cox regression, and least absolute shrinkage and selection operator (LASSO) regression analysis were employed to validate the lncRNA risk model associated with cellular aging. Comparing the infiltration of diverse immune cells enabled the identification of distinct differences in the immunological microenvironments of the two risk groups. Subsequently, we conducted a real-time polymerase chain reaction (qPCR) experiment to confirm the accuracy of the selected lncRNAs. Results: A predictive framework for HCC was constructed based on the expression levels of five lncRNAs. Multivariate and univariate Cox regression analyses revealed that lncRNA signatures associated with senescence were independently correlated with an increased risk of HCC. Additionally, the nomogram also provides a more refined and sensitive model. Further investigation into the variations in immune cells and functions between the high-risk and low-risk groups was conducted. Subsequently, a qPCR experiment results revealed underexpression of AC068756.1, AC090578.1, AC145343.1, and LINC0022 in Huh7 and LM3 cells. In contrast, AP003392.4 did not exhibit a significant difference between Huh7 and control cells. Conclusion: The prognostic features and nomogram, consisting of five aging-related lncRNAs (AC068756.1, AC090578.1, AC145343.1, AP003392.4, and LINC00221), may be useful in predicting the overall survival of HCC.