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doi:10.18632/oncotarget.v8i15

Cited by 6 publications

(3 citation statements)

References 60 publications

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“…The relevance of innate immune pathways in melanoma treatment is highlighted by some immunotherapy approaches such as TLR7 in the adjuvant therapy with imiquimod ( 36 ), TLR9 in the development of the emerging agonists tilsotolimod and vidutolimod ( 37 ), STING in the case of ADU S-100 ( 38 ), and the clinical use of IFN-α ( 39 ). The activation of several innate immune pathways in both tumor cells and other immune cells present in the TME is essential to provide an efficient antitumor response.…”

Section: Discussionmentioning

confidence: 99%

Bacillus Calmette-Guérin immunotherapy induces an efficient antitumor response to control murine melanoma depending on MyD88 signaling

Borges,

Marinho,

Caldeira

et al. 2024

Front. Immunol.

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Bacillus Calmette-Guérin (BCG) is the first line treatment for bladder cancer and it is also proposed for melanoma immunotherapy. BCG modulates the tumor microenvironment (TME) inducing an antitumor effective response, but the immune mechanisms involved still poorly understood. The immune profile of B16-F10 murine melanoma cells was assessed by infecting these cells with BCG or stimulating them with agonists for different innate immune pathways such as TLRs, inflammasome, cGAS-STING and type I IFN. B16-F10 did not respond to any of those stimuli, except for type I IFN agonists, contrasting with bone marrow-derived macrophages (BMDMs) that showed high production of proinflammatory cytokines. Additionally, we confirmed that BCG is able to infect B16-F10, which in turn can activate macrophages and spleen cells from mice in co-culture experiments. Furthermore, we established a subcutaneous B16-F10 melanoma model for intratumoral BCG treatment and compared wild type mice to TLR2-/-, TLR3-/-, TLR4-/-, TLR7-/-, TLR3/7/9-/-, caspase 1-/-, caspase 11-/-, IL-1R-/-, cGAS-/-, STING-/-, IFNAR-/-, MyD88-/-deficient animals. These results in vivo demonstrate that MyD88 signaling is important for BCG immunotherapy to control melanoma in mice. Also, BCG fails to induce cytokine production in the co-culture experiments using B16-F10 and BMDMs or spleen cells derived from MyD88-/- compared to wild-type (WT) animals. Immunotherapy with BCG was not able to induce the recruitment of inflammatory cells in the TME from MyD88-/- mice, impairing tumor control and IFN-γ production by T cells. In conclusion, MyD88 impacts on both innate and adaptive responses to BCG leading to an efficient antitumor response against melanoma.

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Section: Discussionmentioning

confidence: 99%

Bacillus Calmette-Guérin immunotherapy induces an efficient antitumor response to control murine melanoma depending on MyD88 signaling

Borges,

Marinho,

Caldeira

et al. 2024

Front. Immunol.

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“…This, in turn, reduces tumor stiffness and mechanical stress, relieves vascular and lymphatic compression, and enhances drug permeability into tumor tissues ( 67 – 69 ). Currently, antifibrosis drugs such as tranilast, losartan, and pirfenidone, have been used to improve chemotherapy in solid tumors ( 63 , 70 , 71 ), while it warrants subsequent research to confirm their efficacy in glioma. As for stroma-rich tumors, researchers concentrate on developing nanomedicines targeting CAFs to reduce tumor matrix stiffness ( 72 , 73 ).…”

Section: The Chemoresistance Can Be Enhanced By Glioma-associated Fib...mentioning

confidence: 99%

The tumor-associated fibrotic reactions in microenvironment aggravate glioma chemoresistance

Xu,

Zhang,

Chen

et al. 2024

Front. Oncol.

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Malignant gliomas are one of the most common and lethal brain tumors with poor prognosis. Most patients with glioblastoma (GBM) die within 2 years of diagnosis, even after receiving standard treatments including surgery combined with concomitant radiotherapy and chemotherapy. Temozolomide (TMZ) is the first-line chemotherapeutic agent for gliomas, but the frequent acquisition of chemoresistance generally leads to its treatment failure. Thus, it’s urgent to investigate the strategies for overcoming glioma chemoresistance. Currently, many studies have elucidated that cancer chemoresistance is not only associated with the high expression of drug-resistance genes in glioma cells but also can be induced by the alterations of the tumor microenvironment (TME). Numerous studies have explored the use of antifibrosis drugs to sensitize chemotherapy in solid tumors, and surprisingly, these preclinical and clinical attempts have exhibited promising efficacy in treating certain types of cancer. However, it remains unclear how tumor-associated fibrotic alterations in the glioma microenvironment (GME) mediate chemoresistance. Furthermore, the possible mechanisms behind this phenomenon are yet to be determined. In this review, we have summarized the molecular mechanisms by which tumor-associated fibrotic reactions drive glioma transformation from a chemosensitive to a chemoresistant state. Additionally, we have outlined antitumor drugs with antifibrosis functions, suggesting that antifibrosis strategies may be effective in overcoming glioma chemoresistance through TME normalization.

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“…On the other hand, our research group was the first to develop SOCS3 peptidomimetics following a structure-based approach quite similar to that of SOCS1: a long peptide, called KIRESS, exhibited a good affinity for JAK2 and an efficient suppression of IL-22 signaling in keratinocytes, in athymic nude mice with squamous cell carcinoma (SCC) ( 83 ) as well as in primary tumour growth and pulmonary metastasis in triple negative breast cancer (TNBC) models ( 84 ). Similarly, into primary cultured cells, KIRESS reduced the Neural stem cells (NSCs) proliferation via blocking the cell cycle progression from the G0/G1 to S phase and attenuated astrocytic differentiation ( 85 ).…”

Section: Peptidomimetics Targeting Jak-statmentioning

confidence: 99%

Are peptidomimetics the compounds of choice for developing new modulators of the JAK-STAT pathway?

Cugudda,

La Manna,

Marasco

2024

Front. Immunol.

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Protein-protein interactions (PPIs) play critical roles in a wide range of biological processes including the dysregulation of cellular pathways leading to the loss of cell function, which in turn leads to diseases. The dysfunction of several signaling pathways is linked to the insurgence of pathological processes such as inflammation, cancer development and neurodegeneration. Thus, there is an urgent need for novel chemical modulators of dysregulated PPIs to drive progress in targeted therapies. Several PPIs have been targeted by bioactive compounds, and, often, to properly cover interacting protein regions and improve the biological activities of modulators, a particular focus concerns the employment of macrocycles as proteomimetics. Indeed, for their physicochemical properties, they occupy an intermediate space between small organic molecules and macromolecular proteins and are prominent in the drug discovery process. Peptide macrocycles can modulate fundamental biological mechanisms and here we will focus on peptidomimetics active on the Janus kinase/signal transducers and activators of transcription (JAK-STAT) pathways.

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Abstract: The treatment of metastatic androgen-resistant prostate cancer remains a challenge. We describe a protein vector that selectively delivers synthetic dsRNA,

Cited by 6 publications

References 60 publications

Bacillus Calmette-Guérin immunotherapy induces an efficient antitumor response to control murine melanoma depending on MyD88 signaling

Bacillus Calmette-Guérin immunotherapy induces an efficient antitumor response to control murine melanoma depending on MyD88 signaling

The tumor-associated fibrotic reactions in microenvironment aggravate glioma chemoresistance

Are peptidomimetics the compounds of choice for developing new modulators of the JAK-STAT pathway?

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