TY - JOUR
T1 - Let - 7 as biomarker, prognostic indicator, and therapy for precision medicine in cancer
AU - Chirshev, Evgeny
AU - Oberg, Kerby C.
AU - Ioffe, Yevgeniya J.
AU - Unternaehrer, Juli J.
PY - 2019/12
Y1 - 2019/12
N2 - Abnormal regulation and expression of microRNAs (miRNAs) has been documented in various diseases including cancer. The miRNA let ‐ 7 (MIRLET7) family controls developmental timing and differentiation. Let ‐ 7 loss contributes to carcinogenesis via an increase in its target oncogenes and stemness factors. Let ‐ 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 ‐ 7 acts as an oncogene, increasing cancer migration, invasion, chemoresistance, and expression of genes associated with progression and metastasis. Here, we review let ‐ 7 function as tumor suppressor and oncogene, considering let ‐ 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 ‐ 7 family members, pointing to abnormal processes involved in carcinogenesis. Let ‐ 7 is a promising option to complement conventional cancer therapy, but requires a tumor specific delivery method to avoid toxicity. While let ‐ 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 ‐ 7 can be used as a biomarker for rational precision medicine decisions, resulting in improved patient survival.
AB - Abnormal regulation and expression of microRNAs (miRNAs) has been documented in various diseases including cancer. The miRNA let ‐ 7 (MIRLET7) family controls developmental timing and differentiation. Let ‐ 7 loss contributes to carcinogenesis via an increase in its target oncogenes and stemness factors. Let ‐ 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 ‐ 7 acts as an oncogene, increasing cancer migration, invasion, chemoresistance, and expression of genes associated with progression and metastasis. Here, we review let ‐ 7 function as tumor suppressor and oncogene, considering let ‐ 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 ‐ 7 family members, pointing to abnormal processes involved in carcinogenesis. Let ‐ 7 is a promising option to complement conventional cancer therapy, but requires a tumor specific delivery method to avoid toxicity. While let ‐ 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 ‐ 7 can be used as a biomarker for rational precision medicine decisions, resulting in improved patient survival.
UR - https://clintransmed.springeropen.com/track/pdf/10.1186/s40169-019-0240-y
UR - https://www.mendeley.com/catalogue/30f7fcac-9067-38ab-98da-7e62dcb82458/
U2 - 10.1186/S40169-019-0240-Y
DO - 10.1186/S40169-019-0240-Y
M3 - Review article
C2 - 31468250
VL - 8
SP - 24
JO - Clinical and translational medicine
JF - Clinical and translational medicine
IS - 1
ER -