Estrogen 17β‑estradiol accelerates the proliferation of uterine junctional zone smooth muscle cells via the let‑7a/Lin28B axis in adenomyosis.

The estrogen 17β‑estradiol has been proven to serve an indispensable role in the occurrence and development of adenomyosis (ADS). The let‑7a/Lin28B axis can control cell proliferation by acting as a tumor‑inhibiting axis in numerous types of cancer. However, its role in ADS remains unknown. The present study aimed i) to elucidate the role of let‑7a in regulating the proliferation of human uterine junctional zone (JZ) smooth muscle cells (SMCs) in ADS, ii) to evaluate whether 17β‑estradiol modifies the expression levels of let‑7a and Lin28B in JZ SMCs in ADS, and iii) to establish how 17β‑estradiol affects the function of the let‑7a/Lin28B axis in the proliferation of JZ SMCs in ADS. A total of 36 premenopausal women with ADS were enrolled as the experimental group and 34 women without ADS were recruited as the control group. Reverse transcription‑quantitative PCR was used to evaluate the expression level of let‑7a, and western blotting was performed to determine the Lin28B expression levels. Lentiviral null vector, let‑7a overexpression lentiviral vector GV280 and let‑7a inhibition lentiviral vector GV369 were used to infect cells to alter the expression of let‑7a for further functional experiments. 17β‑estradiol and Cell Counting Kit‑8 assays were conducted to determine how 17β‑estradiol affects the function of the let‑7a/Lin28B axis in the proliferation of JZ SMCs in ADS. The results demonstrated that let‑7a was downregulated and Lin28B was upregulated in the JZ SMCs of ADS compared with the control cells (P<0.0001). Moreover, a lower expression of let‑7a led to faster proliferation of JZ SMCs (P<0.05), and 17β‑estradiol affected the let‑7a/Lin28B axis to accelerate the proliferation of JZ SMCs in ADS (P<0.05). These data suggested that 17β‑estradiol collaborates with the let‑7a/Lin28B axis to affect the development of ADS.