Silencing of LLGL2 Suppresses the Estradiol-Induced BPH-1 Cell Proliferation through the Regulation of Autophagy
Lethal giant larvae (Lgl) is an apical-basal polarity gene first identified in <i>Drosophila</i>. LLGL2 is one of the mammalian homologs of Lgl. However, little is known about its function in the prostate. In this study, to explore the new role of LLGL2 in the prostate, we examined the p...
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2022-08-01
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| author | Kyung-Hyun Kim Geum-Lan Hong Yae-Ji Kim Hui-Ju Lee Ju-Young Jung |
| author_facet | Kyung-Hyun Kim Geum-Lan Hong Yae-Ji Kim Hui-Ju Lee Ju-Young Jung |
| author_sort | Kyung-Hyun Kim |
| collection | DOAJ |
| description | Lethal giant larvae (Lgl) is an apical-basal polarity gene first identified in <i>Drosophila</i>. LLGL2 is one of the mammalian homologs of Lgl. However, little is known about its function in the prostate. In this study, to explore the new role of LLGL2 in the prostate, we examined the proliferative activity of a BPH-1 cell line, a well-established model for the human prostate biology of benign prostatic hyperplasia (BPH). The expression of LLGL2 was dose-dependently increased in BPH-1 cells after treatment with 17β-estradiol (E2). Additionally, E2 treatment increased the proliferation of the BPH-1 cells. However, the knockdown of LLGL2 with siRNA significantly suppressed the proliferation of the E2-treated BPH-1 cells. Moreover, si-<i>llgl2</i> treatment up-regulated the expression of LC-3B, ATG7, and p-beclin, which are known to play a pivotal role in autophagosome formation in E2-treated BPH-1 cells. Overexpression of LLGL2 was able to further prove these findings by showing the opposite results from the knockdown of LLGL2 in E2-treated BPH-1 cells. Collectively, our results suggest that LLGL2 is closely involved in the proliferation of prostate cells by regulating autophagosome formation. These results provide a better understanding of the mechanism involved in the effect of LLGL2 on prostate cell proliferation. LLGL2 might serve as a potential target in the diagnosis and/or treatment of human BPH. |
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| language | English |
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| spelling | doaj.art-e62a5b1967e743f39aa393313c5202442023-12-03T13:22:01ZengMDPI AGBiomedicines2227-90592022-08-01108198110.3390/biomedicines10081981Silencing of LLGL2 Suppresses the Estradiol-Induced BPH-1 Cell Proliferation through the Regulation of AutophagyKyung-Hyun Kim0Geum-Lan Hong1Yae-Ji Kim2Hui-Ju Lee3Ju-Young Jung4Department of Veterinary Medicine & Institute of Veterinary Science, Chungnam National University, 99, Daehak-ro, Yuseong-gu, Daejeon 34134, KoreaDepartment of Veterinary Medicine & Institute of Veterinary Science, Chungnam National University, 99, Daehak-ro, Yuseong-gu, Daejeon 34134, KoreaDepartment of Veterinary Medicine & Institute of Veterinary Science, Chungnam National University, 99, Daehak-ro, Yuseong-gu, Daejeon 34134, KoreaDepartment of Veterinary Medicine & Institute of Veterinary Science, Chungnam National University, 99, Daehak-ro, Yuseong-gu, Daejeon 34134, KoreaDepartment of Veterinary Medicine & Institute of Veterinary Science, Chungnam National University, 99, Daehak-ro, Yuseong-gu, Daejeon 34134, KoreaLethal giant larvae (Lgl) is an apical-basal polarity gene first identified in <i>Drosophila</i>. LLGL2 is one of the mammalian homologs of Lgl. However, little is known about its function in the prostate. In this study, to explore the new role of LLGL2 in the prostate, we examined the proliferative activity of a BPH-1 cell line, a well-established model for the human prostate biology of benign prostatic hyperplasia (BPH). The expression of LLGL2 was dose-dependently increased in BPH-1 cells after treatment with 17β-estradiol (E2). Additionally, E2 treatment increased the proliferation of the BPH-1 cells. However, the knockdown of LLGL2 with siRNA significantly suppressed the proliferation of the E2-treated BPH-1 cells. Moreover, si-<i>llgl2</i> treatment up-regulated the expression of LC-3B, ATG7, and p-beclin, which are known to play a pivotal role in autophagosome formation in E2-treated BPH-1 cells. Overexpression of LLGL2 was able to further prove these findings by showing the opposite results from the knockdown of LLGL2 in E2-treated BPH-1 cells. Collectively, our results suggest that LLGL2 is closely involved in the proliferation of prostate cells by regulating autophagosome formation. These results provide a better understanding of the mechanism involved in the effect of LLGL2 on prostate cell proliferation. LLGL2 might serve as a potential target in the diagnosis and/or treatment of human BPH.https://www.mdpi.com/2227-9059/10/8/1981LLGL2benign prostatic hyperplasiaautophagosome formationproliferation |
| spellingShingle | Kyung-Hyun Kim Geum-Lan Hong Yae-Ji Kim Hui-Ju Lee Ju-Young Jung Silencing of LLGL2 Suppresses the Estradiol-Induced BPH-1 Cell Proliferation through the Regulation of Autophagy Biomedicines LLGL2 benign prostatic hyperplasia autophagosome formation proliferation |
| title | Silencing of LLGL2 Suppresses the Estradiol-Induced BPH-1 Cell Proliferation through the Regulation of Autophagy |
| title_full | Silencing of LLGL2 Suppresses the Estradiol-Induced BPH-1 Cell Proliferation through the Regulation of Autophagy |
| title_fullStr | Silencing of LLGL2 Suppresses the Estradiol-Induced BPH-1 Cell Proliferation through the Regulation of Autophagy |
| title_full_unstemmed | Silencing of LLGL2 Suppresses the Estradiol-Induced BPH-1 Cell Proliferation through the Regulation of Autophagy |
| title_short | Silencing of LLGL2 Suppresses the Estradiol-Induced BPH-1 Cell Proliferation through the Regulation of Autophagy |
| title_sort | silencing of llgl2 suppresses the estradiol induced bph 1 cell proliferation through the regulation of autophagy |
| topic | LLGL2 benign prostatic hyperplasia autophagosome formation proliferation |
| url | https://www.mdpi.com/2227-9059/10/8/1981 |
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