Long non‐coding RNA VPS9D1‐AS1 enhances proliferation, invasion, and epithelial‐mesenchymal transition in endometrial cancer via miR‐377‐3p/SGK1
Abstract Endometrial cancer (EC) is a kind of gynecologic malignancy with a rising incidence rate. This study aimed to explore the role of VPS9D1 antisense RNA1 (VPS9D1‐AS1) in EC. The expression of VPS9D1‐AS1, microRNA (miR)‐377‐3p, and serum and glucocorticoid‐regulated kinase 1 (SGK1) was detecte...
| Main Authors: | , , , , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
Wiley
2022-11-01
|
| Series: | Kaohsiung Journal of Medical Sciences |
| Subjects: | |
| Online Access: | https://doi.org/10.1002/kjm2.12606 |
| _version_ | 1797984402667470848 |
|---|---|
| author | Tian‐Fang Peng Yan‐Jie Zhou Jian Zhou Yi Zhou Xin‐Chun Li Qiang Ouyang |
| author_facet | Tian‐Fang Peng Yan‐Jie Zhou Jian Zhou Yi Zhou Xin‐Chun Li Qiang Ouyang |
| author_sort | Tian‐Fang Peng |
| collection | DOAJ |
| description | Abstract Endometrial cancer (EC) is a kind of gynecologic malignancy with a rising incidence rate. This study aimed to explore the role of VPS9D1 antisense RNA1 (VPS9D1‐AS1) in EC. The expression of VPS9D1‐AS1, microRNA (miR)‐377‐3p, and serum and glucocorticoid‐regulated kinase 1 (SGK1) was detected by Quantitative Real‐Time PCR (qRT‐PCR). Cell proliferation, invasion and epithelial‐mesenchymal transition (EMT) were determined by cell counting kit‐8 (CCK‐8), 5‐Ethynyl‐2′‐Deoxyuridine (EdU) transwell, and western bolt. VPS9D1‐AS1 was predicted to sponge miR‐377‐3p via Starbase, and verified by luciferase reporter, RNA binding protein immunoprecipitation (RIP), and RNA pull‐down experiments. The clinical characteristics of VPS9D1‐AS1, miR‐377‐3p, and SGK1 were analyzed. The role of VPS9D1‐AS1 on EC tumorigenesis was assessed in xenografted nude mice. VPS9D1‐AS1 was upregulated in EC cells and tissues. Interference of VPS9D1‐AS1 inhibited growth, invasion, and EMT of EC cells. Mechanically, VPS9D1‐AS1 was a molecular sponge of miR‐377‐3p, and overexpression of miR‐377‐3p reversed VPS9D1‐AS1‐induced EC cells proliferation, invasion, and EMT. Moreover, SGK1 was confirmed to bind with miR‐377‐3p. Furthermore, overexpression of SGK1 alleviated sh‐VPS9D1‐AS1‐caused effects on EC cells. High level of VPS9D1‐AS1 and SGK1, or low miR‐377‐3p expression predicted a poor prognosis. The expression of the three genes was correlated with lymph node metastasis, pathological stage, and International Federation of Gynecology and Obstetrics (FIGO) stage, but not associated with age, ER, and PR expression. Interestingly, knockdown of VPS9D1‐AS1 suppressed EC tumor growth in mice. VPS9D1‐AS1 promoted cell invasion, proliferation, and EMT via modulating miR‐377‐3p/SGK1 axis, which provided new options for therapeutic strategies of EC. |
| first_indexed | 2024-04-11T07:02:20Z |
| format | Article |
| id | doaj.art-57d1c524f5fa4273b28c27377435b97d |
| institution | Directory Open Access Journal |
| issn | 1607-551X 2410-8650 |
| language | English |
| last_indexed | 2024-04-11T07:02:20Z |
| publishDate | 2022-11-01 |
| publisher | Wiley |
| record_format | Article |
| series | Kaohsiung Journal of Medical Sciences |
| spelling | doaj.art-57d1c524f5fa4273b28c27377435b97d2022-12-22T04:38:36ZengWileyKaohsiung Journal of Medical Sciences1607-551X2410-86502022-11-0138111048105910.1002/kjm2.12606Long non‐coding RNA VPS9D1‐AS1 enhances proliferation, invasion, and epithelial‐mesenchymal transition in endometrial cancer via miR‐377‐3p/SGK1Tian‐Fang Peng0Yan‐Jie Zhou1Jian Zhou2Yi Zhou3Xin‐Chun Li4Qiang Ouyang5Department of Gynecological Oncology, Hunan Provincial Tumor Hospital The Affiliated Tumor Hospital of Xiangya Medical School of Central South University Changsha ChinaDepartment of Gynecological Oncology, Hunan Provincial Tumor Hospital The Affiliated Tumor Hospital of Xiangya Medical School of Central South University Changsha ChinaDepartment of Gynecological Oncology, Hunan Provincial Tumor Hospital The Affiliated Tumor Hospital of Xiangya Medical School of Central South University Changsha ChinaDepartment of Gynecological Oncology, Hunan Provincial Tumor Hospital The Affiliated Tumor Hospital of Xiangya Medical School of Central South University Changsha ChinaDepartment of Gynecological Oncology, Hunan Provincial Tumor Hospital The Affiliated Tumor Hospital of Xiangya Medical School of Central South University Changsha ChinaDepartment of Gynecological Oncology, Hunan Provincial Tumor Hospital The Affiliated Tumor Hospital of Xiangya Medical School of Central South University Changsha ChinaAbstract Endometrial cancer (EC) is a kind of gynecologic malignancy with a rising incidence rate. This study aimed to explore the role of VPS9D1 antisense RNA1 (VPS9D1‐AS1) in EC. The expression of VPS9D1‐AS1, microRNA (miR)‐377‐3p, and serum and glucocorticoid‐regulated kinase 1 (SGK1) was detected by Quantitative Real‐Time PCR (qRT‐PCR). Cell proliferation, invasion and epithelial‐mesenchymal transition (EMT) were determined by cell counting kit‐8 (CCK‐8), 5‐Ethynyl‐2′‐Deoxyuridine (EdU) transwell, and western bolt. VPS9D1‐AS1 was predicted to sponge miR‐377‐3p via Starbase, and verified by luciferase reporter, RNA binding protein immunoprecipitation (RIP), and RNA pull‐down experiments. The clinical characteristics of VPS9D1‐AS1, miR‐377‐3p, and SGK1 were analyzed. The role of VPS9D1‐AS1 on EC tumorigenesis was assessed in xenografted nude mice. VPS9D1‐AS1 was upregulated in EC cells and tissues. Interference of VPS9D1‐AS1 inhibited growth, invasion, and EMT of EC cells. Mechanically, VPS9D1‐AS1 was a molecular sponge of miR‐377‐3p, and overexpression of miR‐377‐3p reversed VPS9D1‐AS1‐induced EC cells proliferation, invasion, and EMT. Moreover, SGK1 was confirmed to bind with miR‐377‐3p. Furthermore, overexpression of SGK1 alleviated sh‐VPS9D1‐AS1‐caused effects on EC cells. High level of VPS9D1‐AS1 and SGK1, or low miR‐377‐3p expression predicted a poor prognosis. The expression of the three genes was correlated with lymph node metastasis, pathological stage, and International Federation of Gynecology and Obstetrics (FIGO) stage, but not associated with age, ER, and PR expression. Interestingly, knockdown of VPS9D1‐AS1 suppressed EC tumor growth in mice. VPS9D1‐AS1 promoted cell invasion, proliferation, and EMT via modulating miR‐377‐3p/SGK1 axis, which provided new options for therapeutic strategies of EC.https://doi.org/10.1002/kjm2.12606endometrial cancermiR‐377‐3pSGK1VPS9D1‐AS1 |
| spellingShingle | Tian‐Fang Peng Yan‐Jie Zhou Jian Zhou Yi Zhou Xin‐Chun Li Qiang Ouyang Long non‐coding RNA VPS9D1‐AS1 enhances proliferation, invasion, and epithelial‐mesenchymal transition in endometrial cancer via miR‐377‐3p/SGK1 Kaohsiung Journal of Medical Sciences endometrial cancer miR‐377‐3p SGK1 VPS9D1‐AS1 |
| title | Long non‐coding RNA VPS9D1‐AS1 enhances proliferation, invasion, and epithelial‐mesenchymal transition in endometrial cancer via miR‐377‐3p/SGK1 |
| title_full | Long non‐coding RNA VPS9D1‐AS1 enhances proliferation, invasion, and epithelial‐mesenchymal transition in endometrial cancer via miR‐377‐3p/SGK1 |
| title_fullStr | Long non‐coding RNA VPS9D1‐AS1 enhances proliferation, invasion, and epithelial‐mesenchymal transition in endometrial cancer via miR‐377‐3p/SGK1 |
| title_full_unstemmed | Long non‐coding RNA VPS9D1‐AS1 enhances proliferation, invasion, and epithelial‐mesenchymal transition in endometrial cancer via miR‐377‐3p/SGK1 |
| title_short | Long non‐coding RNA VPS9D1‐AS1 enhances proliferation, invasion, and epithelial‐mesenchymal transition in endometrial cancer via miR‐377‐3p/SGK1 |
| title_sort | long non coding rna vps9d1 as1 enhances proliferation invasion and epithelial mesenchymal transition in endometrial cancer via mir 377 3p sgk1 |
| topic | endometrial cancer miR‐377‐3p SGK1 VPS9D1‐AS1 |
| url | https://doi.org/10.1002/kjm2.12606 |
| work_keys_str_mv | AT tianfangpeng longnoncodingrnavps9d1as1enhancesproliferationinvasionandepithelialmesenchymaltransitioninendometrialcancerviamir3773psgk1 AT yanjiezhou longnoncodingrnavps9d1as1enhancesproliferationinvasionandepithelialmesenchymaltransitioninendometrialcancerviamir3773psgk1 AT jianzhou longnoncodingrnavps9d1as1enhancesproliferationinvasionandepithelialmesenchymaltransitioninendometrialcancerviamir3773psgk1 AT yizhou longnoncodingrnavps9d1as1enhancesproliferationinvasionandepithelialmesenchymaltransitioninendometrialcancerviamir3773psgk1 AT xinchunli longnoncodingrnavps9d1as1enhancesproliferationinvasionandepithelialmesenchymaltransitioninendometrialcancerviamir3773psgk1 AT qiangouyang longnoncodingrnavps9d1as1enhancesproliferationinvasionandepithelialmesenchymaltransitioninendometrialcancerviamir3773psgk1 |