Colorectal cancer (CRC), currently the second most widespread cancer globally, exhibits a higher incidence in young individuals. Advancements have been made in developing anti-colorectal cancer drugs, including cytotoxic chemicals, in the past few decades. There is a need for new and innovative medications to overcome the current challenges in cancer treatment. Recent research examined the efficacy of innovative formulations in the prevention of colorectal cancer. In this study, we evaluated the efficacy of a niosome formulation loaded with Enciprazine hydrochloride (Nio-USAN). We assessed the anti-colorectal cancer characteristics of Nio-USAN by employing several techniques including CCK-8, invasion test, MTT test, flow cytometry, and cell cycle assessment. Quantitative real-time PCR was utilized to assess the transcription of genes linked to apoptosis. The F1-Nio-USAN and F2-Nio-USAN have average sizes of 200 and 500 nm, respectively. The entrapment effectiveness (EE%) of the F1-Nio-USAN and F2-Nio-USAN was measured to be 85.32 ± 0.27 % and 87.12 ± 0.35 %, respectively. The F1-Nio-USAN group exhibited the following percentages of HT-29 cell states: 43 % early apoptosis, 21 % late apoptosis, 7 % necrotic, and 29 % viable. The levels of transcription for cas8, Bid, BAX, cas9, and cas3 were significantly elevated in the treatment groups as compared to the PBS control group (P < 0.001). In addition, the treatment group exhibited significantly reduced levels of BCL2 gene transcription compared to the PBS control group (P < 0.01). These results suggest that it may be possible to improve the efficacy of USAN formulations in combating cancer by utilizing noisome encapsulation.
Colorectal cancer (CRC) remains a significant global health challenge, with an alarming upward trend in Asia. Early detection is crucial for improving outcomes, but there is no consensus on the optimal screening approach. Despite advances in diagnosis and therapy, CRC mortality rates remain substantial. Apoptosis and autophagy, key processes in cancer cell death, exhibit complex molecular crosstalk, particularly involving BH-3-only proteins, which present potential therapeutic targets. Recent studies suggest that manipulating these pathways could enhance cancer treatment by exploiting their regulatory networks. The B-cell lymphoma 2 (BCL-2) family proteins, central to apoptosis regulation, are implicated in CRC initiation, progression, and therapy resistance. BH3-only proteins like BIM and PUMA are linked to caspase-independent cell death, suggesting alternative pathways for CRC treatment and highlighting the potential for targeted therapies. This review provides an overview of CRC management, including the current landscape and challenges of screening programs and delves into the interplay between apoptosis and autophagy in CRC cell death. It emphasizes the critical role of BCL-2 family proteins in CRC pathogenesis and calls for future research to focus on developing non-invasive, cost-effective diagnostic biomarkers, establishing prognostic biomarker panels, and defining predictive biomarkers for existing treatments. These advancements are essential for improving screening strategies, therapeutic interventions, and ultimately, patient outcomes and quality of life.
Because of emerging opportunities for cancer immunotherapy, the capacity to suppress the immune system in order to cure and eradicate cancer is currently a topic of intense study. When the bone marrow microenvironment is exposed to immune suppression, leukemia cells result in the immune system's inability to eliminate malignant cells. To get a better understanding of the immunological possibilities associated with leukemia, clinical trials have explored immunotherapy techniques such as T cell activators, checkpoint inhibitors, antibody medicinal molecules, and cell treatments. One of the most important immune pathways is the programmed cell death 1 (PD1) protein. PD1 is expressed on the surface of T-cells and controls immune reactions. CD274, B7–H1, or PD-L1 are expressed by cells of the myeloid lineage, including macrophages, dendritic cells, effector CD8+ T cells, tumor cells, and tumor-associated suppressor cells. Expression of PD-L1 molecule in cancer has been associated to worse prognosis and resistance to anti-cancer therapies in several malignancies. In this review, we update on the expression of PD-1 molecule in malignant hematological tumor cells and describe these molecules which inhibit the immune response to cancer cells. We provide an overview of the current scientific advancements, the significance of immunotherapy strategies and highlighting the potential for further development in targeting this specific molecule. Additionally, ascertaining if PD-1/PD-L1 can be a reliable prognostic for blood cancer diagnosis.
Colorectal cancer is one of the most prevalent cancers worldwide. An increasing number of cases around the globe are raising concerns for life quality and survival. Various factors including genetic drivers have been extensively studied regarding the disease risk, progression, and metastasis. However, the signaling mechanisms haven't been studied extensively yet. Various therapeutic methods have been established in combating the disease, and mesenchymal stem cells have come up as a crucial cell-based therapeutic strategy. Mesenchymal stem cells have been regarded as potential targets in various cancer types due to their immune-modulatory functions. They can be isolated from many body tissues including bone marrow, peripheral blood, umbilical cord, and adipose tissue. Exosomes derived from mesenchymal stem cells have been reported to affect the expression of certain proteins associated with colorectal cancer. The current review highlights the potential of mesenchymal stem cells and their derived exosomes in treating cancer by causing cytotoxicity and apoptosis. Further, T-cell mediated modulation of exosomes helps reduce the cellular proliferation in cancer cells.