Nat Commun: Double blocking cd47 and HER2 can eliminate radiotherapy resistance in breast cancer cells.

The small simba radiotherapy (RT) has relatively small systemic side effects compared to chemotherapy and is used in all subtypes of breast cancer (BC) treatment.
, however, due to potential tumor radiotherapy resistance, it can eventually lead to recurrence or metastasis of the patient's tumor.
: Nature's current treatment strategy combining RT with Targeted Immunotherapy (TI) is increasingly being used in the treatment of a variety of cancers.
that although targeted immunotherapy can improve the efficacy of tumor radiotherapy, the immunosuppressive effect of radiotherapy on tumor cells still needs further study.
here, we're talking about CD47-mediated anti-devouration in mice treated with radiation resistance breast cancer (BC) cells and RT with the same gene BC as HER2.
expressions of the two receptors were more common in patients with relapsed BC with poor prognostication.
in cells that express HER2, CD47 is given priority, and blocking CD47 or HER2 reduces the cloning originality of both receptors.
CD47 and HER2 gene knock-outs mediated by CRISPR not only inhibit cloning, but also enhance macrophage-mediated attacks.
two receptors in collaboration with RT to control breast tumors in mice with the same gene.
data show that the invasion behavior of radiation-resistant BC is caused by CD47-mediated anti-swallowing effect combined with HER2 to promote proliferation.
in BC radiotherapy, the double blocking of CD47 and HER2 helps eliminate drug-resistant cancer cells.
photo source: NatureCD47 and HER2 Express CD4 in a variety of cancers is a specific antigen expressed in human bone marrow cells, is a specific antigen in human bone marrow cells.
CD47 on tumor cells binds to the ligation SIRP alpha on macrophages, causing phosphorylation at the tail end of the SIRP alpha plasma, which initiates signal cascading that inhibits macrophages' ability to devour.
the purpose of cancer immunotherapy with humanized CD47 antibodies is to enhance the rate of tumor cell removal mediated by macrophages and to show anti-tumor efficacy in toxic human cancers.
, however, in addition to enhancing the phagocation function of tumors, blocking CD47 can also improve the antigen delivery of dc by suppressing EGFR signals, inhibiting the invasion estype of breast cancer stem cells (BCSCs).
based on the study data represents the co-transcription regulation of CD47 and HER2 in radiation-resistant BC cells.
blocking CD47 not only enhances macrophage-mediated phagocytostic phagocytos, but also inhibits HER2-related attacks in radioactively resistant BC cells, which can be reproduced by RT and mice that inhibit the co-inhibition of the two subjects with the gene BC.
results show a potential tumor-promoting growth mechanism, which is due to CD47-enhanced immunity that avoids the effects of her2-promoted intrinsic cell proliferation, leading to aggressive behavior of resistant BC cells.
in BC radiotherapy, double blocking CD47 and HER2 can effectively eliminate drug-resistant cancer cells.
Photo Source: Nature radiation-induced CD47 transcription by HER2-NF-B axis regulation The study found that in radiotherapy-resistant breast cancer (BC) cells, CD47-mediated anti-phagocytic effect increased, while HER2 expression levels also increased.
the co-expression of these two subject proteins is often detected in patients with relapsed BC with poor prognostication.
The expression of CD47 in HER2-expressed cells was prioritized, while blocking the expression of CD47 or HER2 reduced the levels of both proteins, along with a decrease in cell formation capacity and increased phagocytosing.
Photo Source: Nature double-blocking CD47 and HER2 have the same synergetic anti-cancer effects as radiotherapy, and the double-knocking of CD47 and HER2 through CRISPR technology can not only inhibit the formation of cell colonies, but also enhance the ability of macrophages to attack tumor cells.
further studies have shown that in breast tumors in esophageal mice, the double antibodies of these two subject proteins have a synergetic anti-cancer effect with RT.
Photo Source: Nature Radiotherapy Resistance Breast Cancer Cell Model The results show that the aggressive effect of radiotherapy resistant breast cancer cells is caused by CD47-mediated anti-phagocytotic effect and HER2-mediated cell proliferation.
double blocking of CD47 and HER2 can counteract radiotherapy resistance in breast cancer cells.
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