ation using MTT assay (**D**), cell migration (**E**) and invasion (**F**) using Transwell assay were shown. Scale bar: 100 μm. \*p\<0.05, \*\*p\<0.01 vs vector+mimic NC or vector+si-Ctrl; ^&^p\<0.05, ^&&^p\<0.01 vs mimic NC+ HULC or si-Ctrl+HULC.Figure 6HULC silencing inhibited C-33A cell proliferation, migration and invasion through inhibiting TPD52 expression. C-33A cells were co-transfected with si-HULC and TPD52 overexpression vector, and corresponding controls, cell proliferation using MTT assay (**A**), cell migration (**B**) and invasion (**C**) using Transwell assay were shown. Scale bar: 100 μm. \*p\<0.05, \*\*p\<0.01 vs si-Ctrl+vector; ^\#\#^p\<0.01 vs Vector+si-HULC.

Discussion {#S0004}
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In the present work, we report that HULC expression was upregulated in cervical cancer cell lines, and HULC promoted cervical cancer cell proliferation, migration and invasion. Mechanistically, HULC acted as a sponge of miR-218 to elevate expression of TPD52, a target of miR-218, and thereby promoted cervical cancer cell proliferation, migration, and invasion.

As an oncogene, HULC has also been proved to play a critical role in regulating tumor metastasis in colorectal cancer,[@CIT0015] hepatocellular carcinoma,[@CIT0016] and bladder cancer.[@CIT0017] Wang et al revealed that the expression of HULC was upregulated in cervical cancer, and associated with overall survival,[@CIT0011] indicating that HULC may serve as a predictive biomarker for the prognosis of cervical cancer. In the present study, our data also demonstrated that HULC had high expression in cervical cancer cells, which is consistent with the findings showing HULC upregulation in cervical cancer tissues.[@CIT0011] Besides, our results showed that overexpression of HULC significantly promoted cervical cancer cell proliferation, migration and invasion. Our present study further supplements the oncogenic function of HULC in cervical cancer based on the existing literature and supports the view that HULC could act as a potential cervical cancer