Epithelial-mesenchymal transition (EMT) is a biological process that involves the transformation of epithelial cells into more mobile and invasive mesenchymal cells. While EMT is crucial for typical physiological functions like maturation of the embryo and tissue restoration, its association with cancer often leads to tumor proliferation, metastasis, and resistance to therapy. This transition permits tumors to acquire traits that promote invasion, migration, and resistance to cell death. Therefore, unraveling the intricate mechanisms of EMT activation in cancer will contribute to the advancement of personalized medicine and the design of more effective treatments against metastatic disease. Inhibiting EMT holds the potential for restricting cancer cell invasion and metastasis, ultimately improving patient outcomes. EMT induction can be triggered by various factors, including extracellular signals, external substances, and pathological conditions such as hypoxia. This paper primarily examines the function of EMT in the initiation and progression of tumors, along with the factors that contribute to its activation. With the aid of cutting-edge technologies and improved experimental techniques, researchers can more effectively investigate the complex network of molecular events underlying EMT, leading to the identification of novel biomarkers and the advancement of therapies. By leveraging these advancements, scientists are better equipped to unravel the intricacies of EMT and pave the way for advancements in personalized medicine and improved treatment strategies for patients affected by EMT-related conditions. Understanding the cellular events and signaling cascades that drive EMT can aid in the development of interventions that disrupt or reverse this process.
Vafa Meftahpour, T. C. Dakal, Jarek Maciaczyk et al.· Signal Transduction and Targ...· 0 citations
Cancer immunotherapy has substantially advanced cancer treatment, achieving durable responses in select malignancies. However, its widespread application is limited by significant challenges: low efficacy in many solid tumors, severe side effects, and immune evasion facilitated by the tumor microenvironment (TME). Nanotechnology offers a promising approach to address these obstacles. By employing nanoparticles (NPs), we can precisely deliver therapeutics to tumor sites, ensure controlled release to minimize side effects, and amplify the immune response, thereby substantially boosting the effectiveness of immunotherapy. This review comprehensively highlights the latest advancements in using nanotechnology to enhance cancer immunotherapy. This paper details various applications of nanotech in this field. It discusses smart nanoparticles that respond to TME signals to release drugs (e.g., checkpoint inhibitors) directly at the tumor, reducing systemic side effects and activating T-cells. We also explore how nanovaccines, which co-deliver tumor markers and immune boosters, can induce antigen-specific immune responses. Furthermore, mRNA-loaded nanoparticles can directly modify CAR T-cells inside the body, simplifying treatment and increasing efficacy. Strategies like using PLGA NPs to deliver immune enhancers such as IL-2 are also presented, which activate immune cells while minimizing systemic issues. The review also explains how nanoparticles can re-engineer the immunosuppressive TME to create an environment more conducive to immune action. We also emphasize that nanotechnology-enhanced adoptive therapies, particularly cytokine-induced killer (CIK) cell immunotherapy, hold great potential to improve tumor targeting, treatment persistence durability, and overall anticancer efficacy. Collectively, we highlight synergistic effects achieved by combining nanoparticles with other treatments like chemotherapy, radiation, photothermal/photodynamic therapy, and more, which can turn hard-to-treat tumors into susceptible targets. The integration of nanotechnology and immunotherapy holds the potential to meaningfully advance future cancer therapy.
U. Cho, Jingjing Pu, Amit Sharma et al.· Molecular Cancer· 0 citations
The mechanisms through which glioblastoma is initiated, localized, and eludes therapy responses are summarized and an update is provided on recent advances made within this therapeutic space to overcome GBM‐mediated immunosuppression.
Emerson Achari, Farah Ahmady-Nield, Amit Sharma et al.· Immunology and Cell Biology· 0 citations