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Objective: The present work examined the anti-metastatic effects of auraptene and their underlying mechanisms of action in U87 Glioblastoma multiforme (GBM) cells. Materials and Methods: To test the hypothesis, cell culture, Matrigel invasion assay, scratch wound healing assay, gelatin zymography assay, qRT-PCR, and western blot experiments were conducted. Results: At sublethal concentrations of 12.5 and 25 µg/ml, auraptene exhibited a significant reduction in cell invasion and migration of U87 cells, as assessed using scratch wound healing and Transwell tests, respectively. The qRT-PCR and zymography experiments demonstrated a significant decrease in both mRNA expression and activities of MMP-2 and MMP-9 following auraptene treatment. Western blot analysis also showed that MMP-2 protein level and phosphorylation of metastasis-related proteins (p-JNK and p-mTOR) decreased in auraptene-treated cells. Molecular docking studies consistently demonstrated that auraptene exhibits a significant affinity towards MMP-2/-9, the ATP binding site of mTOR and JNK1/2/3. Conclusion: Auraptene inhibited the migration and invasion of GBM cells. This inhibitory effect was induced by modulating specific mechanisms, including suppressing MMPs, JNK, and mTOR activities.
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Neuroblastomas are the most common solid tumors outside of the brain that originate from immature neural crest cells, accounting for about 10% of all pediatric malignancies. The treatment for neuroblastomas involves a multimodal schedule, including surgery, radiation, chemotherapy, and immunotherapy. All these modalities are limited by side effects that might be severe, poor prognosis, and a high risk of recurrence. In the quest for additional therapeutic approaches, phytochemicals have attracted attention owing to their reported antitumor properties, safety, and multimechanistic mode of action. Several studies have used plant-derived bioactive compounds such as phenolics and flavonoids, suggesting modulation of biomolecules and signal transduction pathways involved in neuroblastoma. We reviewed the findings of recent preclinical and clinical studies demonstrating the effects of phytochemicals on neuroblastoma, shedding light on their molecular mechanism of action and potential therapeutic applications.
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[This retracts the article DOI: 10.17179/excli2019-1136.].
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Brain cancers, particularly glioblastoma multiforme (GBM), are challenging health issues with frequent unmet aspects. Today, discovering safe and effective therapeutic modalities for brain tumors is among the top research interests. Immunotherapy is an emerging area of investigation in cancer treatment. Since immune checkpoints play fundamental roles in repressing anti-cancer immunity, diverse immune checkpoint inhibitors (ICIs) have been developed, and some monoclonal antibodies have been approved clinically for particular cancers; nevertheless, there are significant concerns regarding their efficacy and safety in brain tumors. Among the various tools to modify the immune checkpoints, phytochemicals show good effectiveness and excellent safety, making them suitable candidates for developing better ICIs. Phytochemicals regulate multiple immunological checkpoint-related signaling pathways in cancer biology; however, their efficacy for clinical cancer immunotherapy remains to be established. Here, we discussed the involvement of immune checkpoints in cancer pathology and summarized recent advancements in applying phytochemicals in modulating immune checkpoints in brain tumors to highlight the state-of-the-art and give constructive prospects for future research.
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Neoplasias Encefálicas , Inibidores de Checkpoint Imunológico , Compostos Fitoquímicos , Humanos , Compostos Fitoquímicos/uso terapêutico , Compostos Fitoquímicos/farmacologia , Inibidores de Checkpoint Imunológico/uso terapêutico , Inibidores de Checkpoint Imunológico/farmacologia , Neoplasias Encefálicas/tratamento farmacológico , Neoplasias Encefálicas/imunologia , Imunoterapia/métodos , Glioblastoma/tratamento farmacológico , Glioblastoma/imunologia , Transdução de Sinais/efeitos dos fármacos , AnimaisRESUMO
Despite the extensive advancements made in the field of cancer therapy, the outlook of individuals suffering from glioblastoma multiforme remains highly detrimental. The absence of specific treatments for cancerous cells significantly hinders the effectiveness of conventional anticancer techniques. Multiple research studies have demonstrated that the suppression of specific genes or the augmentation of therapeutic proteins through RNA-based therapeutics may represent a valuable approach when combined with chemotherapy or immunotherapy. In recent years, there has been a significant increase in the application of RNA therapeutics in conjunction with chemotherapy and immunotherapy. This emerging field has become a prominent area of research for advancing various types of cancer treatments. The present investigation provides an in-depth overview of the classification and application of RNA therapy, focusing on the mechanisms of RNA antitumor treatment and the current status of clinical studies on RNA drugs.
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Glioblastoma , Glioma , Humanos , RNA , Glioma/genética , Glioma/terapia , Glioma/patologia , Glioblastoma/tratamento farmacológico , Glioblastoma/metabolismo , Glioblastoma/patologia , Imunoterapia/métodosRESUMO
Liposomal drug delivery systems stand as versatile therapeutic platforms for precisely targeting related elements in cancerous tissues owing to their intrinsic passive and acquired active targeting capabilities and exceptional compatibility with physiologic environments. When the capacity of liposomes as nanocarriers is combined with the revolutionary potential of RNA therapies in affecting undruggable targets, the outcome would be promising drug candidates as game-changers in the cancer treatment arena. However, optimizing liposome composition, physicochemical properties, and surface chemistry is paramount to maximizing their pharmacokinetic and pharmacodynamic attributes. This review highlighted the potential of liposomes as nanovehicles for RNA therapeutics through a literature review and looked at the most recent preclinical and clinical advancements in utilizing liposomal RNA therapeutics for cancer management. Notably, the discovery of novel targets, advancements in liposome engineering, and organizing well-planned clinical trials would help uncover the incredible potential of these nanotherapeutics in cancer patients.
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Lipossomos , Neoplasias , Humanos , Lipossomos/uso terapêutico , Sistemas de Liberação de Medicamentos , Neoplasias/tratamento farmacológicoRESUMO
There are increasing incidences and mortality rates for colorectal cancer in the world. It is common for chemotherapy and radiation given to patients with colorectal cancer to cause toxicities that limit their effectiveness and cause cancer cells to become resistant to these treatments. Additional targeted treatments are needed to improve patient's quality of life and outcomes. Immunotherapy has rapidly emerged as an incredibly exciting and promising avenue for cancer treatment in recent years. This innovative approach provides novel options for tackling solid tumors, effectively establishing itself as a new cornerstone in cancer treatment. Specifically, in the realm of colorectal cancer (CRC), there is great promise in developing new drugs that target immune checkpoints, offering a hopeful and potentially transformative solution. While immunotherapy of CRC has made significant advances, there are still obstacles and limitations. CRC patients have a poor response to treatment because of the immune-suppressing function of their tumor microenvironment (TME). In addition to blocking inhibitory immune checkpoints, checkpoint-blocking antibodies may also boost immune responses against tumors. The review summarizes recent advances in immune checkpoint inhibitors (ICIs) for CRC, including CTLA-4, PD-1, PD-L1, LAG-3, and TIM-3.
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Neoplasias Colorretais , Qualidade de Vida , Humanos , Imunoterapia , Neoplasias Colorretais/terapia , Microambiente TumoralRESUMO
It has been understood for nearly a century that patients with intestinal inflammatory disease (IBD) have a higher risk of developing colorectal cancer (CRC). Recently, two species of lactic acid bacteria, Lactobacillus plantarum and Lactococcus lactis, have been investigated as therapeutic agents for IBD. These bacteria have been shown to survive gastric transit, to adhere and colonize in the intestinal tract of humans and modulate the intestinal microbiota and immune response. L. plantarum and L. lactis might be used as multifunctional drugs for the treatment of IBD and the prevention or treatment of CRC. This article summarizes current knowledge of L. plantarum and L. lactis as therapeutic and preventative agents for IBD and CRC, respectively.
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Neoplasias Colorretais , Microbioma Gastrointestinal , Doenças Inflamatórias Intestinais , Lactobacillus plantarum , Lactococcus lactis , Humanos , Doenças Inflamatórias Intestinais/tratamento farmacológico , Doenças Inflamatórias Intestinais/microbiologia , Intestinos , Lactobacillus plantarum/fisiologia , Neoplasias Colorretais/tratamento farmacológico , Neoplasias Colorretais/prevenção & controleRESUMO
The most common primary brain malignancy, glioblastoma multiforme, is tremendously resistant to conventional treatments due to its potency for metastasis to surrounding brain tissue. Temozolomide is a chemotherapeutic agent that currently is administrated during the treatment procedure. Studies have attempted to investigate new agents with higher effectiveness and fewer side effects. Combretastatin A-4 (CA-4), a natural compound derived from Combretum caffrum, has been recently considered for its potent antitumor activities in a wide variety of preclinical solid tumor models. Our findings have shown that CA-4 exerts potent anti-proliferative and apoptotic effects on glioma cells, and ROS generation may be involved in these cellular events. CA-4 has imposed G2 arrest in U-87 cells. We also observed that CA-4 significantly reduced the migration and invasion capability of U-87 cells. Furthermore, the gene expression and enzyme activity of MMP-2 and MMP-9 were significantly inhibited in the presence of CA-4. We also observed a considerable decrease in PI3K and Akt protein expression following treatment with CA-4. In conclusion, our findings showed significant apoptogenic and anti-metastatic effects of CA-4 on glioma cells and also suggested that the PI3K/Akt/MMP-2/-9 and also ROS pathway might play roles in these cellular events.
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Neoplasias Encefálicas , Glioma , Humanos , Metaloproteinase 2 da Matriz/metabolismo , Proteínas Proto-Oncogênicas c-akt/metabolismo , Transdução de Sinais , Fosfatidilinositol 3-Quinases/metabolismo , Espécies Reativas de Oxigênio , Proliferação de Células , Glioma/patologia , Apoptose , Neoplasias Encefálicas/patologia , Linhagem Celular TumoralRESUMO
Standard cancer chemotherapeutics often produce significant adverse effects and eventually lose their effectiveness due to the emergence of resistance mechanisms. As a result, patients with malignant tumors experience a poor quality of life and a short lifespan. Thus, combination medication regimens provide various advantages, including increased success rate, fewer side effects, and fewer occurrences of resistance. Curcumin (Cur), a potential phytochemical from turmeric, when coupled with traditional chemotherapeutics, has been established to improve the effectiveness of cancer treatment in clinical and preclinical investigations. Cur not only exerts multiple mechanisms resulting in apoptotic cancer cell death but also reduces the resistance to standard chemotherapy drugs, mainly through downregulating the multi-drug resistance (MDR) cargoes. Recent reports showed the beneficial outcomes of Cur combination with many chemotherapeutics in various malignancies. Nevertheless, owing to the limited bioavailability, devising co-delivery strategies for Cur and conventional pharmaceuticals appears to be required for clinical settings. This review summarized various Cur combinations with standard treatments as cancer therapeutics.
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Osteosarcoma (OS) is the most prevalent primary bone cancer, with a high morbidity and mortality rate. Over the past decades, therapeutic approaches have not considerably improved patients' survival rates, and further research is required to find efficient treatments for OS. Data from several studies have shown that urolithin B (UB), the intestinal metabolite of polyphenolic ellagitannins, is emerging as a new class of anticancer compounds, yet its effect on OS cancer cells remains elusive. Herein, we investigated UB's antimetastatic, antiproliferative, and apoptotic effects on the MG-63 OS cell line. Cell viability assay, annexin V/propidium iodide staining, cell cycle arrest analysis, determination of the gene expression of MMP-2, MMP-9, Bax, Bcl-2, and p53 messenger RNA (mRNA), evaluation of reactive oxygen species (ROS) generation and migration, and MMP-2 and MMP-9 protein expression assessments were performed. UB caused late apoptosis, necrosis, G2/M arrest, and ROS generation in MG-63 cells. It increased the mRNA expression of the p53 tumor suppressor and Bax proapoptotic genes. UB also inhibited the migration and metastatic behavior of MG-63 OS cells by downregulating mRNA and MMP-2 and MMP-9 protein expression. In general, although further in vivo investigations are warranted, the current results showed that UB might be utilized as a potential novel natural compound for OS therapy due to its nontoxic, antiproliferative, and antimetastatic nature.
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Apoptose , Osteossarcoma , Humanos , Proteína Supressora de Tumor p53 , Metaloproteinase 9 da Matriz/genética , Metaloproteinase 9 da Matriz/metabolismo , Metaloproteinase 2 da Matriz/genética , Metaloproteinase 2 da Matriz/metabolismo , Espécies Reativas de Oxigênio/metabolismo , Proteína X Associada a bcl-2/metabolismo , Pontos de Checagem da Fase G2 do Ciclo Celular , Linhagem Celular Tumoral , Necrose , Proliferação de Células , Osteossarcoma/metabolismo , RNA Mensageiro , Movimento CelularRESUMO
Human T lymphotropic virus type 1 (HTLV-1) infection can cause adult T-cell lymphoblastic leukemia (ATLL), an incurable, chemotherapy-resistant malignancy. In a quest for new therapeutic targets, our study sought to determine the levels of AKT, mTOR, and PI3K in ATLL MT-2 cells, HTLV-1 infected NIH/3T3 cells (Inf-3T3), and HTLV-1 infected patients (Carrier, HAM/TSP, and ATLL). Furthermore, the effects of rigosertib, wortmannin, and rapamycin on the PI3K/Akt/mTOR pathway to inhibit the proliferation of ATLL cells were examined. The results showed that mRNA expression of Akt/PI3K/mTOR was down-regulated in carrier, HAM/TSP, and ATLL patients, as well as MT-2, and Inf-3T3 cells, compared to the healthy individuals and untreated MT-2 and Inf-3T3 as controls. However, western blotting revealed an increase in the phosphorylated and activated forms of AKT and mTOR. Treating the cells with rapamycin, wortmannin, and rigosertib decreased the phosphorylated forms of Akt and mTOR and restored their mRNA expression levels. Using these inhibitors also significantly boosted the expression of the pro-apoptotic genes, Bax/Bcl-2 ratio as well as the expression of the tumor suppressor gene p53 in the MT-2 and Inf-3T3cells. Rigosertib was more potent than wortmannin and rapamycin in inducing sub-G1 and G2-M cell cycle arrest, as well as late apoptosis in the Inf-3T3 and MT-2 cells. It also synergized the cytotoxic effects of vincristine. These findings demonstrate that HTLV-1 downregulation of the mRNA level may occur as a negative feedback response to increased PI3K-Akt-mTOR phosphorylation by HTLV-1. Therefore, using rigosertib alone or in combination with common chemotherapy drugs may be beneficial in ATLL patients.
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Infecções por HTLV-I , Vírus Linfotrópico T Tipo 1 Humano , Leucemia-Linfoma de Células T do Adulto , Adulto , Animais , Camundongos , Humanos , Leucemia-Linfoma de Células T do Adulto/tratamento farmacológico , Leucemia-Linfoma de Células T do Adulto/genética , Leucemia-Linfoma de Células T do Adulto/metabolismo , Sirolimo/farmacologia , Wortmanina , Proteínas Proto-Oncogênicas c-akt/genética , Proteínas Proto-Oncogênicas c-akt/metabolismo , Fosfatidilinositol 3-Quinases , Infecções por HTLV-I/genética , Serina-Treonina Quinases TOR/genética , RNA MensageiroRESUMO
Regarding the multimechanistic nature of cancers, current chemo- or radiotherapies often fail to eradicate disease pathology, and frequent relapses or resistance to therapies occur. Brain malignancies, particularly glioblastomas, are difficult-to-treat cancers due to their highly malignant and multidimensional biology. Unfortunately, patients suffering from malignant tumors often experience poor prognoses and short survival periods. Thus far, significant efforts have been conducted to discover novel and more effective modalities. To that end, modulation of the ubiquitin-proteasome system (UPS) has attracted tremendous interest since it affects the homeostasis of proteins critically engaged in various cell functions, for example, cell metabolism, survival, proliferation, and differentiation. With their safe and multimodal actions, phytochemicals are among the promising therapeutic tools capable of turning the operation of various UPS elements. The present review, along with an updated outline of the role of UPS dysregulation in multiple cancers, provided a detailed discussion on the impact of phytochemicals on the UPS function in malignancies, especially brain tumors.
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Neoplasias Encefálicas , Ubiquitina , Humanos , Ubiquitina/genética , Ubiquitina/metabolismo , Complexo de Endopeptidases do Proteassoma/metabolismo , Inibidores de Proteassoma/farmacologia , Inibidores de Proteassoma/uso terapêutico , Recidiva Local de Neoplasia/tratamento farmacológico , Neoplasias Encefálicas/tratamento farmacológico , Compostos Fitoquímicos/farmacologia , Compostos Fitoquímicos/uso terapêuticoRESUMO
Glioblastoma multiforme (GBM) is the most aggressive kind of malignant primary brain tumor in humans. Given the limitation of Conventional therapeutic strategy, the development of nanotechnology and natural product therapy seems to be an effective method enhancing the prognosis of GBM patients. In this research, cell viability, mRNA expressions of various apoptosis-related genes apoptosis, and generation of reactive oxygen species (ROS) in human U-87 malignant GBM cell line (U87) treated with Urolithin B (UB) and CeO2-UB. Unlike CeO2-NPs, both UB and CeO2-UB caused a dose-dependent decrease in the viability of U87 cells. The half-maximal inhibitory concentration values of UB and CeO2-UB were 315 and 250 µM after 24 h, respectively. Moreover, CeO2-UB exerted significantly higher effects on U87 viability, P53 expression, and ROS generation. Furthermore, UB and CeO2-UB increased the accumulation of U87 cells in the SUB-G1 population, decreased the expression of cyclin D1, and increased the Bax/Bcl2 ratio expression. Collectively, these data indicate that CeO2-UB exhibited more substantial anti-GBM effects than UB. Although further in vivo investigations are needed, these results proposed that CeO2-NPs could be utilized as a potential novel anti-GBM agent after further studies.
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Glioblastoma , Nanopartículas , Humanos , Espécies Reativas de Oxigênio/metabolismo , Glioblastoma/tratamento farmacológicoRESUMO
Prostate cancer is one of the main global health threats for men which is in close association with chronic inflammation. Neuropeptide substance P (SP), acting through neurokinin receptor (NK-1R), induces various pro-inflammatory responses which are strongly involved in the pathogenesis of several diseases as well as cancer. Therefore, we aimed to investigate the pro-inflammatory functions of the SP/NK1R complex in prostate cancer and the therapeutic effects of its inhibition by NK-1R antagonist, aprepitant, in vitro. MTT assay was conducted for the cytotoxicity assessment of aprepitant in prostate cancer cells. The protein expression levels were evaluated by Western blot assay. Quantitative real-time PCR (qRT-PCR) was applied to measure mRNA expression levels of pro-inflammatory cytokines. Concurrently, the protein concentrations of pro-inflammatory cytokines were also analyzed by enzyme-linked immunosorbent assay. We observed that SP increased the levels of pro-inflammatory cytokines (IL-1ß, IL-6, and TNF-α), while treatment with aprepitant reduced the effects of SP. We also indicated that SP increased the protein levels of nuclear factor-kappa B (NF-κB), as the main regulator of inflammatory processes, and also an NF-κB target gene, cyclooxygenase 2 (COX-2) in prostate cancer cells, while treatment with aprepitant reversed these effects. Taken together, our findings highlight the importance of the SP/NK1R system in the modulation of pro-inflammatory responses in prostate cancer cells and suggest that aprepitant may be developed as a novel anti-inflammatory agent for the management of cancer-associated inflammation.
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NF-kappa B , Neoplasias da Próstata , Masculino , Humanos , NF-kappa B/genética , NF-kappa B/metabolismo , Substância P/metabolismo , Substância P/farmacologia , Substância P/uso terapêutico , Transdução de Sinais , Aprepitanto/farmacologia , Aprepitanto/uso terapêutico , Inflamação/tratamento farmacológico , Inflamação/metabolismo , Interleucina-1beta/metabolismo , Interleucina-1beta/farmacologia , Interleucina-1beta/uso terapêutico , Neoplasias da Próstata/tratamento farmacológico , Neoplasias da Próstata/genéticaRESUMO
Discovering novel cancer therapies has attracted extreme interest in the last decade. In this regard, multidrug resistance (MDR) to chemotherapies is a key challenge in cancer treatment. Cancerous cells are growingly become resistant to existing chemotherapeutics by employing diverse mechanisms, highlighting the significance of discovering approaches to overcome MDR. One promising strategy is utilizing aptamers as unique tools to target elements or signaling pathways incorporated in resistance mechanisms, or develop actively targeted drug delivery systems or chimeras enabling the precise delivery of novel agents to inhibit the conventionally undruggable resistance elements. Furthermore, due to their advantages over their proteinaceous counterparts, particularly antibodies, including improved targeting action, enhanced thermal stability, easier production, and superior tumor penetration, aptamers are emerging and have frequently been considered for developing cancer therapeutics. Here, we highlighted significant chemoresistance pathways in cancer and discussed the use of aptamers as prospective tools to surmount cancer MDR.
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Resistencia a Medicamentos Antineoplásicos , Neoplasias , Humanos , Sistemas de Liberação de Medicamentos , Neoplasias/tratamento farmacológico , Neoplasias/patologiaRESUMO
BACKGROUND: Harmaline is a ß-carboline alkaloid that can be extracted from the seeds of Peganum harmala. Harmaline has been shown to exhibit a potent cytotoxic effect against tumor cells. In this study, the anti-glioblastoma activity of harmaline was investigated in vitro. METHODS AND RESULTS: Cell viability, apoptosis, and cell cycle arrest were assessed in U-87 cells treated with harmaline at different doses. Reactive oxygen species (ROS) generation and the mRNA expression of apoptosis-associated genes were assessed. The anti-metastatic effect of harmaline on U-87 cells was evaluated by gelatin zymography assay where matrix metalloproteinase [MMP]-2/-9 enzymatic activity was measured, and the scratch assay was used to assess migratory responses. Flow cytometry demonstrated that harmaline could suppress the proliferation and induce sub-G1 cell cycle arrest and apoptotic cell death in glioblastoma cells. Harmaline treatment was also associated with an upregulation of the cell cycle-related genes, p21 and p53, and pro-apoptotic Bax, as well as the induction of ROS. The zymography assay indicated that the essential steps of metastasis were potently suppressed by harmaline through inhibiting the expression of MMP-2 and - 9. In addition, the migration of U-87 cells was significantly reduced after harmaline treatment. CONCLUSION: Our data suggest a basis for further research of harmaline which has potential cytotoxic activities in glioblastoma cells; inducing cell cycle arrest and apoptosis, repression of migration, possibly invasion, and metastasis.
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Antineoplásicos , Glioblastoma , Humanos , Harmalina/farmacologia , Linhagem Celular Tumoral , Espécies Reativas de Oxigênio/farmacologia , Antineoplásicos/farmacologia , Glioblastoma/tratamento farmacológico , Apoptose , Proliferação de CélulasRESUMO
In terms of frequency and aggressiveness, glioblastoma multiforme (GBM) is undoubtedly the most frequent and fatal primary brain tumor. Despite advances in clinical management, the response to current treatments is dismal, with a 2-year survival rate varying between 6 and 12 percent. Metformin, a derivative of biguanide widely used in treating type 2 diabetes, has been shown to extend the lifespan of patients with various malignancies. There is limited evidence available on the long-term survival of GBM patients who have taken metformin. This research examined the literature to assess the connection between metformin's anticancer properties and GBM development. Clinical findings, together with the preclinical data from animal models and cell lines, are included in the present review. This comprehensive review covers not only the association of hyperactivation of the AMPK pathway with the anticancer activity of metformin but also other mechanisms underpinning its role in apoptosis, cell proliferation, metastasis, as well as its chemo-radio-sensitizing behavior against GBM. Current challenges and future directions for developments and applications of metformin-based therapeutics are also discussed.
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Neoplasias Encefálicas , Diabetes Mellitus Tipo 2 , Glioblastoma , Metformina , Animais , Metformina/farmacologia , Metformina/uso terapêutico , Glioblastoma/metabolismo , Diabetes Mellitus Tipo 2/tratamento farmacológico , Proliferação de Células , Neoplasias Encefálicas/tratamento farmacológico , Neoplasias Encefálicas/patologia , Linhagem Celular TumoralRESUMO
The immune system's role in maintaining the health of the gastrointestinal (GI) system is like a double-edged sword. Simultaneously, it could reduce the risk of pathogen invasion by the inflammatory response. However, if regulated improperly, it could also propagate oncogenic signaling that transfers a normal cell into the malignant counterpart. Thus, several mechanisms have been proposed, such as the immune system could disturb the GI homeostasis and increase the survival and proliferative capacity of cells, leading to the formation of a wide range of malignancies. Among the endless list of these mechanisms, inflammatory responses are currently fascinating research areas, as this response regulation is by the gut microbiota. Given this, microbiota manipulation might be a convenient and efficient way to prevent GI cancer. Probiotics could potentially achieve this by overturning the milieu in favor of normal gut homeostasis. In addition to the safety of the use of probiotics, along with their potential ability to interact with immune system responses, these bacteria are also being analyzed from the perspective of dietary supplements. In the present review, we aimed to look into the mechanisms through which probiotics modulate immune response to stimulate anti-inflammatory responses and promote immune surveillance against neoplastic cells.