Research articleLong non-coding RNA ABHD11-AS1 facilitates the progression of cervical cancer by competitively binding to miR-330–5p and upregulating MARK2
Graphical abstract
Section snippets
Background
As the primary malignant tumor of the cervix, cervical cancer (CC) is among the most prevalent gynecological malignant tumors, which threatens the health of women around the globe [1]. CC is the second leading cause of death among female malignancies in China [2]. About 130,000 women in China are diagnosed with CC every year with about 53,000 deaths [3]. Besides human papillomavirus (HPV) which is regarded as the most critical etiological element in CC development, genetic variations also play
Cell culture
Human CC cell line HeLa, human papillomavirus (HPV)-18 immortalized cell line, CaSki (HPV16-positive CC cell line), C-33A (HPV-negative CC cell line), HCC94 (well-differentiated CC cell line) and the normal cervical epithelial cell line (End1/E6E7) were utilized for our study. End1/E6E7, HeLa, C-33A and CaSki cells were purchased from American Type Culture Collection (ATCC) (Manassas, VA, USA). HCC94 cells were brought from Procell Life Science & Technology Co., Ltd. (Wuhan, China). End1/E6E7
ABHD11-AS1 depletion attenuates CC cell malignant behaviors
First, since ABHD11-AS1 is an antisense lncRNA, we identified its full-length sequence by 5′ and 3’ RACE experiment, and the results were shown in Fig. S1A. Then, to explore the association between ABHD11-AS1 and CC in vitro, we detected ABHD11-AS1 expression in different cell lines. Supported by the results of RT-qPCR, we found that ABHD11-AS1 level in CC cell lines (HCC94, HeLa, C-33A and CaSki) was higher than End1/E6E7 cells (Fig. 1A). Later, functional assays were implemented with the
Discussion
Cervical cancer (CC) is a notorious malignancy with high morbidity and mortality prevalent in the whole world [1]. With the wide coverage of early screening and the development of treatment, the survival rate of CC patients has risen. Nevertheless, for advanced patients, the overall treatment efficacy is still not ideal [5], indicating a demand for consistent molecular research on CC progression. For the past few years, a great number of lncRNAs were found to be correlated with CC development [
Conclusions
In sum, our study elucidated that ABHD11-AS1 sponged miR-330–5p to upregulate MARK2 so as to facilitate cell growth, migration, invasion and decline apoptosis of CC cells. Though clinical samples were not involved, the current study could still offer a novel sight for understanding CC.
Ethics approval and consent to participate
Not applicable.
Consent for publication
Not applicable.
Availability of data and materials
Not applicable.
Authors’ contributions
SH designed this study. SH, XZ and JY performed experiment, prepared figures, interpreted data. JY wrote the draft. All authors have read and approved the manuscript.
Funding
This work was supported by Clinical Medical Centers of Suzhou (SZZX201505); Introduce Project of Clinical Medical Experts of Suzhou (SZYJTD201707); Suzhou Municipal Hospital Gynecological Clinical Trial and Improvement Project (SLT201955); Suzhou Science and Technology Project (SYSD2018124).
A. RT-qPCR tested ABHD11-AS1 expression in CC cells (HCC94, HeLa, C-33A, and CaSki) versus normal control cells (End1/E6E7). B. ABHD11-AS1 expression was quantified via RT-qPCR in CC cells with transfection
Declaration of competing interest
None.
Acknowledgments
We are very grateful for the support of the laboratory and the help of the team colleagues.
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