Background: AdipoR2belongs to seven transmembrane domains receptor family, which has been shown to have played an important role in the development of human tumor, but the underlying mechanisms are poorly understood. In this study, we found that AdipoR2 expression correlates with glioma grade. In addition, we also investigated the mechanisms behind the anti-proliferative effects of AdipoR2 in U251 cells (human glioma cell line) using the colony formation assay and WST-8 growth assay.
Methods: U251 cell line were cultured in vitro; Western Blotting was used to detect the expression of related proteins; Using Quantitative RT-PCR to detect AdipoR1and AdipoR2 expression; Detection of Cell cycle assay by flow cytometry; The gene expression profiles of glioma samples from CCGA were analyzed by Matlab and GSEA software.
Results: We found 648 upregulated genes and 436 downregulated genes correlated with AdipoR2 expression in 158 glioma samples. GSEA analysis suggested that AdipoR2 is a cell cycle–associated gene. Results of flow cytometry analysis indicated that AdipoR2 induced cell cycle G0/G1 arrest in U251 cells. Furthermore, we identified the AMPK/mTOR signaling axis to be involved in AdipoR2-induced cell cycle arrest.
Conclusions: Our results suggest that AdipoR2 may represent a novel endogenous negative regulator of GBM cell proliferation. These findings also suggested that AdipoR2may be a promising therapeutic target in GBM patients.

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On 11 Feb, 2021
Received 31 Jan, 2021
On 25 Jan, 2021
On 23 Jan, 2021
Invitations sent on 22 Jan, 2021
On 22 Jan, 2021
Received 22 Jan, 2021
On 19 Jan, 2021
On 19 Jan, 2021
On 19 Jan, 2021
Posted 27 Dec, 2020
On 27 Dec, 2020
Received 26 Dec, 2020
On 16 Dec, 2020
Invitations sent on 16 Dec, 2020
On 16 Dec, 2020
On 16 Dec, 2020
On 16 Dec, 2020
Posted 11 Dec, 2020
On 11 Dec, 2020
On 11 Dec, 2020
On 11 Dec, 2020
Posted 12 Nov, 2020
On 24 Nov, 2020
Received 23 Nov, 2020
Invitations sent on 08 Nov, 2020
On 08 Nov, 2020
On 04 Nov, 2020
On 04 Nov, 2020
On 04 Nov, 2020
On 03 Nov, 2020
On 11 Feb, 2021
Received 31 Jan, 2021
On 25 Jan, 2021
On 23 Jan, 2021
Invitations sent on 22 Jan, 2021
On 22 Jan, 2021
Received 22 Jan, 2021
On 19 Jan, 2021
On 19 Jan, 2021
On 19 Jan, 2021
Posted 27 Dec, 2020
On 27 Dec, 2020
Received 26 Dec, 2020
On 16 Dec, 2020
Invitations sent on 16 Dec, 2020
On 16 Dec, 2020
On 16 Dec, 2020
On 16 Dec, 2020
Posted 11 Dec, 2020
On 11 Dec, 2020
On 11 Dec, 2020
On 11 Dec, 2020
Posted 12 Nov, 2020
On 24 Nov, 2020
Received 23 Nov, 2020
Invitations sent on 08 Nov, 2020
On 08 Nov, 2020
On 04 Nov, 2020
On 04 Nov, 2020
On 04 Nov, 2020
On 03 Nov, 2020
Background: AdipoR2belongs to seven transmembrane domains receptor family, which has been shown to have played an important role in the development of human tumor, but the underlying mechanisms are poorly understood. In this study, we found that AdipoR2 expression correlates with glioma grade. In addition, we also investigated the mechanisms behind the anti-proliferative effects of AdipoR2 in U251 cells (human glioma cell line) using the colony formation assay and WST-8 growth assay.
Methods: U251 cell line were cultured in vitro; Western Blotting was used to detect the expression of related proteins; Using Quantitative RT-PCR to detect AdipoR1and AdipoR2 expression; Detection of Cell cycle assay by flow cytometry; The gene expression profiles of glioma samples from CCGA were analyzed by Matlab and GSEA software.
Results: We found 648 upregulated genes and 436 downregulated genes correlated with AdipoR2 expression in 158 glioma samples. GSEA analysis suggested that AdipoR2 is a cell cycle–associated gene. Results of flow cytometry analysis indicated that AdipoR2 induced cell cycle G0/G1 arrest in U251 cells. Furthermore, we identified the AMPK/mTOR signaling axis to be involved in AdipoR2-induced cell cycle arrest.
Conclusions: Our results suggest that AdipoR2 may represent a novel endogenous negative regulator of GBM cell proliferation. These findings also suggested that AdipoR2may be a promising therapeutic target in GBM patients.

Figure 1

Figure 1

Figure 2

Figure 2

Figure 3

Figure 3

Figure 4

Figure 4
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