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Retinoic acid early transcript 1K (RAET1K) is a long noncoding RNA located on chromosome 6q25.1, comprising four exons and approximately 1,883 base pairs[1]. It is significantly upregulated in tumor tissues, especially in lung adenocarcinoma and acute myeloid leukemia, and is correlated with poor patient prognosis[1][3]. Functionally, RAET1K acts as a competitive endogenous RNA (ceRNA), sponging microRNAs such as miR-135a-5p (in lung adenocarcinoma) or miR-503-5p (in AML) to regulate downstream targets like cyclin E1 (CCNE1) and inositol polyphosphate-4-phosphatase type II (INPP4B), promoting cell cycle progression, cell proliferation, and inhibiting apoptosis. Its dysregulation is implicated in cancer initiation and progression, and may serve as both a prognostic biomarker and a candidate therapeutic target in malignancies[1][3].
ceRNA mechanism: RAET1K acts as a sponge for specific microRNAs (miR-135a-5p in lung adenocarcinoma; miR-503-5p in acute myeloid leukemia), leading to upregulation of target mRNAs (such as CCNE1 and INPP4B) that promote cell cycle progression and inhibit apoptosis
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