Abnormal regulation and expression of microRNAs (miRNAs) has been documented in various diseases including cancer. The miRNA
let
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7
(MIRLET7) family controls developmental timing and differentiation.
Let
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7
loss contributes to carcinogenesis via an increase in its target oncogenes and stemness factors.
Let
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7
targets include genes regulating the cell cycle, cell signaling, and maintenance of differentiation. It is categorized as a tumor suppressor because it reduces cancer aggressiveness, chemoresistance, and radioresistance. However, in rare situations
let
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7
acts as an oncogene, increasing cancer migration, invasion, chemoresistance, and expression of genes associated with progression and metastasis. Here, we review
let
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7
function as tumor suppressor and oncogene, considering
let
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7
as a potential diagnostic and prognostic marker, and a therapeutic target for cancer treatment. We explain the complex regulation and function of different
let
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7
family members, pointing to abnormal processes involved in carcinogenesis.
Let
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7
is a promising option to complement conventional cancer therapy, but requires a tumor specific delivery method to avoid toxicity. While
let
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7
therapy is not yet established, we make the case that assessing its tumor presence is crucial when choosing therapy. Clinical data demonstrate that
let
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7
can be used as a biomarker for rational precision medicine decisions, resulting in improved patient survival.