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CD73 as a potential opportunity for cancer immunotherapy
Ghasem Ghalamfarsa1, Mohammad Hossein Kazemi2,3, Sahar Raoofi Mohseni2
1a Cellular and Molecular Research Center , Yasuj University of Medical Sciences , Yasuj , Iran.
Introduction:
Cancer cells apply various mechanisms to induce and enhance immune escape. The complex network of immune-response modulating factors in the tumor microenvironment is a reason for the difficulties encountered when attempting to treat many cancers. Adenosine is a potent immune-modulating factor that can be generated through the degradation of ATP by cooperative action of NTPDase1 (CD39) and ecto-5'-nucleotidase (CD73) molecules. Overexpression of CD73 on tumor and immune cells leads to the presence of a high concentration of this factor in the tumor region. Upregulation of CD73 is associated with the overproduction of adenosine; it suppresses antitumor immune responses and helps proliferation, angiogenesis, and metastasis. Areas covered: We attempt to clarify the immunobiology of CD73 in association with its role in cancer development, angiogenesis, and metastasis. Moreover, we have reviewed CD73-targeting studies and highlighted CD73 as a potent target for cancer immunotherapy. Expert opinion: It seems that blockade of CD73, in combination with immune checkpoint inhibitors such as anti-PD-L1 and anti-CTLA-4, can be a novel promising therapeutic strategy that can be evaluated in the future trials.
Insights
CD73 overexpression in tumors fuels cancer growth and immune evasion by producing adenosine. Blocking CD73 may enhance cancer immunotherapy when combined with immune checkpoint inhibitors.
Area of Science:
- Immunology
- Oncology
- Biochemistry
Background:
- Cancer cells utilize immune escape mechanisms within the tumor microenvironment, complicating treatment.
- Adenosine, produced by CD39 and CD73, is a key immune-modulating factor in tumors.
- CD73 overexpression elevates adenosine, suppressing anti-tumor immunity and promoting cancer progression, angiogenesis, and metastasis.
Purpose of the Study:
- To elucidate the immunobiology of CD73 in cancer development, angiogenesis, and metastasis.
- To review existing CD73-targeting strategies for cancer immunotherapy.
- To highlight CD73 as a promising therapeutic target.
Main Methods:
- Literature review of CD73's role in cancer.
- Analysis of CD73's association with tumor progression and immune evasion.
- Evaluation of CD73-targeting studies in cancer immunotherapy.
Main Results:
- CD73 overexpression is linked to increased adenosine levels in the tumor microenvironment.
- Adenosine produced by CD73 suppresses anti-tumor immune responses.
- CD73 contributes to cancer proliferation, angiogenesis, and metastasis.
Conclusions:
- CD73 plays a significant role in cancer immune evasion and progression.
- Targeting CD73 presents a potential strategy for enhancing cancer immunotherapy.
- Combination therapy with CD73 blockade and immune checkpoint inhibitors (e.g., anti-PD-L1, anti-CTLA-4) shows promise for future clinical trials.
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