Cancer, a pervasive threat to human health, presents formidable challenges to traditional treatment approaches. Tumor immunotherapy has emerged as a promising strategy for combating malignancies by bolstering the body's immune response to thwart tumor metastasis and recurrence. Nonetheless, the intricacies of tumors, patient heterogeneity, and the presence of tumor-immunosuppressive microenvironments have limited the overall efficacy of immunotherapy, achieving only approximately a 20% success rate. In recent years, nanomaterials have garnered increasing attention in the realm of tumor immunotherapy due to their inherent advantages, such as excellent biocompatibility, precise targeting, and controlled drug release. Nanomaterials empower immunostimulatory molecules and therapeutic agents with the ability to specifically target tumors, amplify drug accumulation at tumor sites, facilitate local immune modulation, alleviate immunosuppressive microenvironments, and thereby enhance the effectiveness of tumor immunotherapy. This review provides an overview of the current state of immunotherapy and offers insights into the ongoing research progress surrounding various nanomaterials aimed at augmenting the efficacy of immunotherapy.

Cancer treatment faces multiple challenges, including tumor heterogeneity, drug resistance, microenvironment influence, treatment side effects, and treatment cost. The heterogeneity of the tumor makes the effect of the same treatment vary in different patients, so the development of personalized treatment strategies is crucial. In addition, resistance of tumor cells to therapeutic drugs is a major challenge, and new strategies to overcome resistance are needed. As a cutting-edge field of science and technology, nanotechnology has brought great potential and opportunities for tumor treatment. Nanoparticle drug delivery systems improve drug efficacy and reduce side effects through precise targeted delivery and controlled release. Cell-membrane coated nanoparticles show great promise in tumor therapy. Nanoparticles coated with cell membranes have good biocompatibility, can reduce the obstacles of immune rejection and cell uptake, improve the accumulation and retention of drugs in tumor tissues, and have good drug delivery ability, drug stability and control release ability. This review discusses advances in the use of cell-membrane coated nanoparticles to target tumor drugs.

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.

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.

As an important part of Traditional Chinese Medicine (TCM) inspection, face diagnosis is significant in judging the rise and fall of viscera and essence and diagnosing and treating diseases. Cancer is a serious disease that endangers human life and health. Face diagnosis can play a great role in diagnosing and treating tumors, but this approach has not achieved the expected effects due to the lack of research. Herein, we summarized the research regarding facial expression, color, shape, and state, demonstrating that facial diagnosis is significant in diagnosing and treating tumors. We also propose that facial diagnosis must be combined with computer technology to realize the objectification of facial diagnosis as soon as possible to play a greater role in diagnosing and treating tumors.

Nanozyme with biomimetic enzyme activity has the advantages of good catalytic performance, high stability, and is not easily affected by temperature. However, the application of tumor microenvironment (TME) in the tumor is limited due to its low catalytic activity. Herein, a multifunctional nanozyme based on CuCoP with multivalent metal ions (Cu+/Cu2+ and Co2+/ Co3+) provides an innovative strategy for constructing acid-responsive cancer therapy. CuCoP has excellent photothermal properties (photothermal conversion efficiency of 66.9%) as well as glutathione (GSH) peroxidase activity and high photo-enhanced peroxidase-like (POD) enzyme activity in weak acid TME. CuCoP can consume the overexpressed GSH, thus alleviating the antioxidant capacity of the tumor, and reduces Cu2+/ Co3+ to Cu+/ Co 2+. Subsequently, the generated Cu+/Co2+ will react with endogenous H2O2 to generate cytotoxic hydroxyl radical (•OH), which have high catalytic efficiency in weakly acidic TME. Crucially, the synergistic effect of PTT and the cascade reaction of bimetallic atoms with GSH and H2O2 can effectively reduce antioxidant capacity, inhibit tumors and trigger effective immune cell death (ICD) process, which caused a strong immune response and inhibit tumor recurrence and metastasis. As a novel bimetallic sulfide nanoenzyme triggered by TME, CuCoP has great research value in cancer therapy.

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.

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.

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.

Cancer is the leading cause of death in the world, throughout the global researches of cancer treatment, people have a deeper understanding of cancer, and the treatment methods are constantly breakthrough. Conventional surgery, chemotherapy and radiotherapy have serious adverse effects and patients' quality of life is not significantly improved. Now, photodynamic therapy, photothermal therapy andthermodynamic therapy based on nanotechnology and materials technology are booming, and the development of these novel cancer therapies and their combination therapies brings more possibilities for cancer treatment. This review summarizes the research progress of novel cancer therapies based on nano and material technology from the aspects of mechanism of action and therapeutic methods, hoping to provide reference for their clinical application.

Breast cancer, as a malignant tumor with easy metastasis and poor prognosis, threatens the health of women around the world. Increasing studies have shown that the Bcl-2 family of apoptosis-related proteins is often expressed abnormally in breast cancer. The Bcl-2 homology 3 (BH3) mimetic peptide can bind and neutralize Bcl-2, preventing its binding to the apoptosis "effector" proteins Bak and Bax, thereby promoting the apoptosis process. However, there is a lack of effective intracellular delivery system for BH3 to exert its biological activity. Therefore, this study utilized an activatable supercharged polypeptide (ASCP) tumor-targeted delivery platform based on pH and protease response to achieve the targeted release of BH3 at the tumor site. Ultimately, intracellular delivery of BH3 was achieved and induced apoptosis of breast tumor cells, preventing the development of breast cancer.

Protein S-nitrosylation (SNO), emerging as an important posttranslational modification, involves covalent addition of nitric oxide (NO) to the sulfur atom of cysteine in proteins. Accumulated evidence suggests that protein SNO plays crucial roles in pathophysiological mechanisms in cancer, which is attracting great attention. However, there are still controversies about whether S-nitrosylated proteins act as oncogenic proteins or tumor suppressors in cancer. In this review, we provide an overview of the early and latest evidence regarding the underlying mechanism and dual roles of SNO in cancer, in an effort to clarify its contribution in tumor progression. It has been well established that S-nitrosylated proteins restrain tumor progression in several types of cancer, while they have exhibited activities in promoting cell proliferation and inhibiting apoptosis in some other kinds of cancer. Interestingly, emerging evidence also has highlighted both its anti-cancer and pro-tumorigenic roles in several other cancer diseases. Finally, current limitations and future research prospects are presented. The overview of targeting SNO in cancer will provide new opportunities for drug development through in-depth exploration of SNO-mediated signaling pathways.

Macrophages are a type of white blood cells that can exist in two different functional states, known as M1 and M2. M1 macrophages secrete pro-inflammatory cytokines that can promote tumor growth and metastasis, whereas M2 macrophages secrete anti-inflammatory cytokines that can inhibit tumor progression. This phenomenon, referred to as macrophage polarization, has been implicated in the development and progression of cancer. Furthermore, macrophage polarization is currently being investigated in the context of COVID-19 severity. It is believed that M1 macrophages may contribute to the excessive inflammation observed in severe COVID-19 cases, while M2 macrophages may confer protection against the disease. Hence, comprehending the role of macrophage polarization in both cancer and COVID-19 has the potential to enhance treatment strategies for both conditions.

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.

Alternative bio actively chemicals may be found in natural goods and traditional herb medications, but only a few plant-information formulations have been rigorously studied and verified for their potential as medicinal therapies. The study of plant-derived elements' immunomodulation capabilities and their ability as provoke the immune system as combat various elemental disorders like cancer is, nonetheless, a promising area in current therapeutics information on plant-derived chemicals. This research showed how network pharmacology may be applied as define and validate natural individual elements or more complicated preparations as prospective cancer therapies information on their various aim capabilities in this research. We give a summary of the present state of understanding on network pharmacology, with a particular emphasis on various technical methods and their implications for cancer treatment.

Lung cancer is the leading cause of cancer-related deaths. Non-small cell lung cancer (NSCLC) accounts for about 85% of all lung cancers, and lung adenocarcinoma is the most common NSCLC. Most patients with lung cancer eventually lead to local and metastatic recurrence, including many patients who have completely removed the primary tumor during surgery and have no noticeable metastasis. There are two different deoxynucleotide triphosphate (dNTP) libraries in eukaryotic cells. The de novo synthesis of dNTPs in the cytoplasm is coordinated with the cell cycle and reaches a peak in the S phase, thereby providing deoxynucleotides for the replication of genomic DNA. In contrast, the mitochondrial pool of dNTPs is maintained through the mitochondrial deoxynucleoside rescue pathway throughout the cell cycle and is essential for mtDNA replication. Mitochondria are vital cell powers in assimilation and catabolism. Oxidative phosphorylation (OXPHOS) of mitochondria is essential for the self-renewal of cancer stem-like cells in lung cancer, glioblastoma and leukemia. Thymidine kinase 2 (TK2) and deoxyguanosine kinase (DGUOK) are two mitochondrial deoxynucleoside kinases, which are responsible for the transport of pyrimidine and purine deoxynucleoside in mitochondria. Apoptosis and autophagy are important processes that regulate cell proliferation and death in normal cells and cancer cells. Inducing cancer cell apoptosis and autophagy is an effective means to treat malignant tumors. This review discusses the research progress of the relationship between mitochondrial deoxyguanosine kinase and lung adenocarcinoma cell apoptosis and autophagy.

Despite the advantages of nanoscale drug delivery systems, traditional nanoparticles often encounter challenges such as detection and elimination by the immune system. To circumvent these limitations, scientists have created biomimetic nanoparticles that extend circulation time, decrease clearance rates, and optimize drug delivery. The integration of cell membranes onto nanoparticle surfaces yields Cell Membrane-coated Nanoparticles (CMNPs) that exhibit behavior akin to actual cells while offering superior structural robustness and stability. A variety of cell membranes, including those of red blood cells, white blood cells, and cancer cells, lend unique properties and targeting capabilities to CMNPs. This review outlines the diagnostic and therapeutic roles of CMNP-based drug delivery systems in oncology and contemplates their possible clinical impact.

 In the past, researchers investigated the immune response acting against mycobacterial antigens in tuberculosis (TB). Several ELISA tests have been conducted for the diagnosis of tuberculosis. Other researchers manipulated 16 kDa antigen from Mycobacterium Tuberculosis to develop a tuberculosis diagnostic test while some others studied the subspecies of M. tuberculosis. In the present study, we explored the possibilities of detecting 16 kDa protein derived from M. tuberculosis, on an interdigitated electrode (IDE). Measurements with Electrochemical impedance spectroscopy and current-volt systems were demonstrated using antibody as the probe.  Further, the involvement of gold nanoparticle for the signal-enhancement and high-performance are evidenced. The specificity in the serum containing samples is used to show the clinical relevancy. 16 kDa antigen used in this experiment is highly reliable for TB diagnosis as it largely expresses and can be implemented in other sensing system.

Tripartite motif-containing (TRIM) proteins consist of over 80 proteins, the majority of which exhibit E3 ubiquitin ligase activity. E3 ligases have a critical role in various cellular processes by specifically recognizing and ubiquitinating substrate proteins to promote their proteasomal degradation or alter their activities. Numerous studies have indicated that TRIMs are involved in carcinogenesis through various mechanisms. However, the regulatory mechanisms delimitating TRIMs’ function as E3 ligases has not yet been specifically addressed in a previous review article. In this review, we focus on recent advancements in understanding how certain TRIMs function solely as E3 ligases during cancer cell proliferation, apoptosis, and metastasis. We comprehensively summarize the target proteins of TRIMs involved in disordered signaling pathways such as Wnt/β-catenin, PI3K/AKT, NF-κB, p53, ERK, and STAT3, as well as those regulating the cell cycle and glycolysis. Following ubiquitination modification by TRIM E3 ligases, these target proteins either undergo proteasome-mediating degradation, maintain steady levels, or get activated/inactivated. This review provides a foundation for the development of E3 ligase-based cancer treatments.

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.