CD73 is a glycosylphosphatidylinositol (GPI) anchored cell surface protein, also known as ecto-5’-nucleotidase (ecto-5’-NT, EC 3.1.3.5). Accumulating data have shown that CD73 play important roles during cancer growth and metastasis [
1‐
3]. CD73 has both enzymatic and non-enzymatic functions [
4]. As an enzyme, CD73 catalyzes the AMP breakdown into adenosine. Notably, adenosine is an important purine signaling molecule which has been found to be involved in tumor immunoescape [
5]. In addition to its enzymatic function, CD73 is also a regulatory molecule which related to cancer invasive and metastatic properties [
3,
6,
7]. Studies have found that CD73 can promote proliferation and migration of several types of cancer cells [
6,
8‐
10]. Cervical cancer, a cancer arising from cervix is due to the abnormal proliferation of cells that have the ability to evade growth suppression. Cervical cancer is high in the rank of cancers affect women, with both the fourth-highest incidence and the fourth-highest fatality rate among women worldwide [
11]. Infection with several special types of human papilloma virus (HPV) has been found to be the most high-risk cause of cervical cancer [
12]. However, HPV infection was not enough to trigger cervical cancer. Other factors, like molecular alteration have also been found to play important role during cervical cancer development [
13,
14]. The role of CD73 in cervical cancer cells has not been well studied. In the present study, we investigated the effect of CD73 overexpression on cervical cancer cells proliferation and migration, and further explored its underlying regulatory mechanisms. Our data demonstrated that CD73 overexpression promoted Hela and SiHa cells proliferation and migration. Moreover, this promotive effect of CD73 should be via an enzymatic activity independent mechanism.