LncRNA DUXAP8 induces breast cancer radioresistance by modulating the PI3K/AKT/mTOR pathway and the EZH2-E-cadherin/RHOB pathway
Radiation resistance poses a major clinical challenge in breast cancer (BC) treatment, but little is known about how long noncoding RNA (lncRNA) may regulate this phenomenon. Here, we reported that DUXAP8 was highly expressed in radioresistant BC tissues, and high expression of DUXAP8 was associated...
| Main Authors: | , , , , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Taylor & Francis Group
2022-12-01
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| Series: | Cancer Biology & Therapy |
| Subjects: | |
| Online Access: | http://dx.doi.org/10.1080/15384047.2022.2132008 |
| _version_ | 1797404061127933952 |
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| author | Changjiang Lei Shaoting Li Ying Fan Li Hua Qingyun Pan Yuan Li Zhixiong Long Rui Yang |
| author_facet | Changjiang Lei Shaoting Li Ying Fan Li Hua Qingyun Pan Yuan Li Zhixiong Long Rui Yang |
| author_sort | Changjiang Lei |
| collection | DOAJ |
| description | Radiation resistance poses a major clinical challenge in breast cancer (BC) treatment, but little is known about how long noncoding RNA (lncRNA) may regulate this phenomenon. Here, we reported that DUXAP8 was highly expressed in radioresistant BC tissues, and high expression of DUXAP8 was associated with poor prognosis. We found that the overexpression of DUXAP8 promoted radioresistance, while the knockdown of DUXAP8 expression increased radiosensitivity. Further studies revealed that DUXAP8 enhanced the radioresistance of BC cells by activating the PI3K/AKT/mTOR pathway and by repressing the expression of E-cadherin and RHOB through interaction with EZH2. Together, our work demonstrates that the overexpression of DUXAP8 promotes the resistance of BC cells toward radiation through modulating PI3K/AKT/mTOR pathway and EZH2-E-cadherin/RHOB axis. Targeting DUXAP8 may serve as a potential strategy to overcome radioresistance in BC treatment. |
| first_indexed | 2024-03-09T02:47:40Z |
| format | Article |
| id | doaj.art-a7d43be86b45424b86ac1335870a9f26 |
| institution | Directory Open Access Journal |
| issn | 1538-4047 1555-8576 |
| language | English |
| last_indexed | 2024-03-09T02:47:40Z |
| publishDate | 2022-12-01 |
| publisher | Taylor & Francis Group |
| record_format | Article |
| series | Cancer Biology & Therapy |
| spelling | doaj.art-a7d43be86b45424b86ac1335870a9f262023-12-05T15:58:14ZengTaylor & Francis GroupCancer Biology & Therapy1538-40471555-85762022-12-0123111310.1080/15384047.2022.21320082132008LncRNA DUXAP8 induces breast cancer radioresistance by modulating the PI3K/AKT/mTOR pathway and the EZH2-E-cadherin/RHOB pathwayChangjiang Lei0Shaoting Li1Ying Fan2Li Hua3Qingyun Pan4Yuan Li5Zhixiong Long6Rui Yang7the Fifth Hospital of Wuhanthe Fifth Hospital of Wuhanthe Fifth Hospital of Wuhanthe Fifth Hospital of Wuhanthe Fifth Hospital of Wuhanthe Fifth Hospital of Wuhanthe Fifth Hospital of Wuhanthe Fifth Hospital of WuhanRadiation resistance poses a major clinical challenge in breast cancer (BC) treatment, but little is known about how long noncoding RNA (lncRNA) may regulate this phenomenon. Here, we reported that DUXAP8 was highly expressed in radioresistant BC tissues, and high expression of DUXAP8 was associated with poor prognosis. We found that the overexpression of DUXAP8 promoted radioresistance, while the knockdown of DUXAP8 expression increased radiosensitivity. Further studies revealed that DUXAP8 enhanced the radioresistance of BC cells by activating the PI3K/AKT/mTOR pathway and by repressing the expression of E-cadherin and RHOB through interaction with EZH2. Together, our work demonstrates that the overexpression of DUXAP8 promotes the resistance of BC cells toward radiation through modulating PI3K/AKT/mTOR pathway and EZH2-E-cadherin/RHOB axis. Targeting DUXAP8 may serve as a potential strategy to overcome radioresistance in BC treatment.http://dx.doi.org/10.1080/15384047.2022.2132008lncrna duxap8aktezh2breast cancerradioresistance |
| spellingShingle | Changjiang Lei Shaoting Li Ying Fan Li Hua Qingyun Pan Yuan Li Zhixiong Long Rui Yang LncRNA DUXAP8 induces breast cancer radioresistance by modulating the PI3K/AKT/mTOR pathway and the EZH2-E-cadherin/RHOB pathway Cancer Biology & Therapy lncrna duxap8 akt ezh2 breast cancer radioresistance |
| title | LncRNA DUXAP8 induces breast cancer radioresistance by modulating the PI3K/AKT/mTOR pathway and the EZH2-E-cadherin/RHOB pathway |
| title_full | LncRNA DUXAP8 induces breast cancer radioresistance by modulating the PI3K/AKT/mTOR pathway and the EZH2-E-cadherin/RHOB pathway |
| title_fullStr | LncRNA DUXAP8 induces breast cancer radioresistance by modulating the PI3K/AKT/mTOR pathway and the EZH2-E-cadherin/RHOB pathway |
| title_full_unstemmed | LncRNA DUXAP8 induces breast cancer radioresistance by modulating the PI3K/AKT/mTOR pathway and the EZH2-E-cadherin/RHOB pathway |
| title_short | LncRNA DUXAP8 induces breast cancer radioresistance by modulating the PI3K/AKT/mTOR pathway and the EZH2-E-cadherin/RHOB pathway |
| title_sort | lncrna duxap8 induces breast cancer radioresistance by modulating the pi3k akt mtor pathway and the ezh2 e cadherin rhob pathway |
| topic | lncrna duxap8 akt ezh2 breast cancer radioresistance |
| url | http://dx.doi.org/10.1080/15384047.2022.2132008 |
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