Natural products have been an invaluable and useful source of anticancer agents over the years. Several compounds have been synthesized from natural products by modifying their structures or by using naturally occurring compounds as building blocks in the synthesis of these compounds for various purposes in different fields, such as biology, medicine, and engineering. Multiple modern and costly treatments have been applied to combat cancer and limit its lethality, but the results are not significantly refreshing. Natural products, which are a significant source of new therapeutic drugs, are currently being investigated as potential cytotoxic agents and have shown a positive trend in preclinical research and have prompted numerous innovative strategies in order to combat cancer and expedite the clinical research. Natural products are becoming increasingly important for drug discovery due to their high molecular diversity and novel biofunctionality. Furthermore, natural products can provide superior efficacy and safety due to their unique molecular properties. The objective of the current review is to provide an overview of the emergence of natural products for the treatment and prevention of cancer, such as chemosensitizers, immunotherapeutics, combinatorial therapies with other anticancer drugs, novel formulations of natural products, and the molecular mechanisms underlying their anticancer properties.

/pdf/natural-products-as-anticancer-agents-current-status-and-22j65xxx.pdf

Natural Products as Anticancer Agents: Current Status and Future Perspectives

Esophageal cancer (EC) is the eighth most common type of cancer worldwide and ranks sixth among the causes of cancer-related mortality. Due to the high mortality rate and poor treatment efficacy for EC, millions of individuals succumb to this disease; thus, the identification of novel treatment targets is of utmost importance and urgency. In recent years, there have been advances if therapies targeting cell cycle regulators. p21 is a type of cell cycle regulator that plays a dual role in tumor cells, as it can not only regulate the cell cycle, induce apoptosis and inhibit cell proliferation, but can also protect cells from apoptosis. It has been found that p21 often exerts a tumor-suppressive effect on EC, which provides a basis for its use as a treatment target for EC. Therefore, the aim of the present study was to review the function of p21 and its potential value as a therapeutic target for EC.

/pdf/function-of-p21-and-its-therapeutic-effects-in-esophageal-5ehyu5hryd.pdf

Function of p21 and its therapeutic effects in esophageal cancer (Review)

Cinobufagin restrains the growth and triggers DNA damage of human hepatocellular carcinoma cells via proteasome-dependent degradation of thymidylate synthase.

Cancer is a major public health concern worldwide; it is the second-highest cause of death in the United States. According to projections of cancer incidence and mortality rates throughout the world for the year 2023, triple-negative breast cancer (TNBC) is expected to be the leading cause of cancer related death among women worldwide. Traditional strategies for the treatment of TNBC have many drawbacks, such as drug resistance, toxicity etc. Discovering novel treatment delivery techniques and researching innovative, efficient drug delivery methods is important. This review discusses the types and subtypes of TNBC. The problems associated with standard therapies, mechanism of drug resistance for TNBC and highlights the need to develop novel therapeutic strategies. It provides information on the relative prevalence and severity of TNBC in the world of cancer. Several treatment approaches viz. targeted therapy, gene therapy, bacterial-mediated therapy, nanomedicine, immune checkpoint inhibitors, theranostic, radiotherapy, chemotherapy, immunotherapy, herbal therapy, and AI-based treatment for TNBC, are discussed in detail. Additionally, diagnostic techniques, including imaging and biopsy, gene expression profiling, mammography, magnetic resonance imaging, ultrasound, computed tomography scan, positron emission tomography scan, and immunohistochemistry, have been discussed in the review for effective cancer treatment. This in-depth analysis highlights the need for innovative and individualized TNBC care methods to serve patients better. 

Recent advancements in nanoconstructs for the theranostics applications for triple negative breast cancer

It is well established that gastrointestinal (GI) cancers are common and devastating diseases around the world. Despite the significant progress that has been made in the treatment of GI cancers, the mortality rates remain high, indicating a real need to explore the complex pathogenesis and develop more effective therapeutics for GI cancers. G protein-coupled receptors (GPCRs) are critical signaling molecules involved in various biological processes including cell growth, proliferation, and death, as well as immune responses and inflammation regulation. Substantial evidence has demonstrated crucial roles of GPCRs in the development of GI cancers, which provided an impetus for further research regarding the pathophysiological mechanisms and drug discovery of GI cancers. In this review, we mainly discuss the roles of sphingosine 1-phosphate receptors (S1PRs), angiotensin II receptors, estrogen-related GPCRs, and some other important GPCRs in the development of colorectal, gastric, and esophageal cancer, and explore the potential of GPCRs as therapeutic targets.

Roles of G Protein-Coupled Receptors (GPCRs) in Gastrointestinal Cancers: Focus on Sphingosine 1-Shosphate Receptors, Angiotensin II Receptors, and Estrogen-Related GPCRs.

Protease-activated receptor 2 (PAR-2) has been demonstrated to promote invasion and metastasis of certain cancer cells. This study aimed to investigate the mechanism by which PAR-2 regulated invasion and migration of esophageal cancer (EC) cells EC109. A successfully constructed PAR-2 shRNA lentiviral vector (Lenti-PAR-2 shRNA) was stably transfected into EC109 cells, and the expression of PAR-2 in infected cells was detected by quantitative real-time PCR (qRT-PCR) and western blotting. Specific inhibitors, PD98059 (for MEK/ERK) and LY294002 (for PI3K/Akt), were used to confirm the role of MEK/ERK and PI3K/Akt signaling pathways, respectively, in PAR-2-regulated invasion and migration of EC109 cells. A significant decrease in PAR-2 mRNA and protein expression was detected in EC109 cells stably transfected with Lenti-PAR-2 shRNA. The PAR-2 agonist could dramatically promote cell invasion and migration, up-regulate the expression of MMP-9 and TM4SF3, and activate MEK/ERK and PI3K/Akt signaling pathways. However, PAR-2 gene silencing attenuated PAR-2-mediated enhancement of invasion and migration of EC109 cells, significantly down-regulated the mRNA and protein expression of MMP-9 and TM4SF3, and inhibited ERK (Try202/204) and Akt (Ser473) phosphorylation. An effect similar to PAR-2 silencing could be achieved with the two specific MEK/ERK and PI3K/Akt pathway inhibitors. Consequently, these results demonstrated that PAR-2 promoted invasion and migration of esophageal cancer cells EC109 by activating MEK/ERK and PI3K/Akt signaling pathways, which was accompanied by up-regulation of MMP-9 and TM4SF3 expression. Hence, PAR-2 may be a potential candidate for anti-metastasis treatment of EC.

PAR-2 promotes invasion and migration of esophageal cancer cells by activating MEK/ERK and PI3K/Akt signaling pathway.

Secretory breast carcinoma (SBC) is one of the rarest breast carcinomas and currently lacks a standard treatment regimen. To date, few reports on double primary SBCs have been published, especially regarding the tumors’ genomic features. A 51-year-old woman with early SBC who developed a secondary SBC in the contralateral mammary tissue 140 months later was evaluated. Here, we describe for the first time the sequencing results of a Chinese patient with nonsimultaneous double-primary SBC. In addition to the ETV6-NTRK3 fusion, variants in polymorphisms of enzymes related to drug metabolism variant genes, including BCL2L11, CYP2B6, CYP2C19, ERCC1, GSTM1, GSTP1, MTHFR, NQO1, TYMS, and XRCC, were present according to 425-gene DNA sequencing. The ETV6-NTRK3 fusion site was different between the tumors; furthermore, whole-gene exon sequencing revealed that genetic variation spectrum of the two tumors was different. A POLDIP2 mutation was found in the first tumor, and HDLBP, MMP2, PLEKHA6 and ZNF285 variants were detected in the second tumor. Our findings further our understanding of the molecular pathogenesis of SBCs, especially regarding tumors occurring at different times in one patient. Further molecular analyses of such cases are warranted to improve targeted therapies for SBC. 

The genomic profile of double primary secretory breast carcinoma in one patient provides evidence for the treatment of such carcinoma: A case report.

Cinobufagin isolated from traditional Chinese herbs has antitumour, anaesthetic, analgesic and anti-inflammatory effects. Recently, the antitumour activity of cinobufagin has attracted increasing attention from researchers. However, the anticancer activity of this drug on esophageal cancer cells and the precise mechanism are unclear. In this study, we determined the inhibitory effect of cinobufagin on the growth of three esophageal squamous cell carcinoma cell lines and explored its underlying mechanism. EC-109, Kyse-150, and Kyse-520 cells were treated with different concentrations of cinobufagin. The results of the Cell Counting Kit-8 (CCK-8) and clone formation assays showed that cinobufagin significantly reduced cell proliferation in a dose- and time-dependent manner. Also, flow cytometry and Hoechst 33342 staining indicated that the inhibition of growth induced by cinobufagin was mediated by G2/M cell cycle arrest and apoptosis. In addition, the expression of proteins related to cell cycle arrest and apoptosis was assessed by real-time quantitative (q)RT-PCR and Western blot. The results showed that cinobufagin caused G2/M arrest via upregulation of p21 and Wee1 and downregulation of cyclin B1 and Cdc2 at the mRNA and protein levels and induced apoptosis via upregulation of cleaved caspase-3, Puma and Noxa expression and an increased Bax/Bcl-2 ratio. Other data further showed that cinobufagin increased p73 expression and decreased Mdm2 expression, whereas p53 expression was not significantly changed. Taken together, these results suggest that growth inhibition of cinobufagin in esophageal cancer cells might act through the p73 pathway and its downstream molecules.

Cinobufagin Promotes Cell Cycle Arrest and Apoptosis to Block Human Esophageal Squamous Cell Carcinoma Cells Growth via the p73 Signalling Pathway.

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PAR-2 promotes invasion and migration of esophageal cancer cells by activating MEK/ERK and PI3K/Akt signaling pathway.

The genomic profile of double primary secretory breast carcinoma in one patient provides evidence for the treatment of such carcinoma: A case report.

Cinobufagin Promotes Cell Cycle Arrest and Apoptosis to Block Human Esophageal Squamous Cell Carcinoma Cells Growth via the p73 Signalling Pathway.