Long non‑coding RNA PTCSC3 suppresses triple‑negative breast cancer by downregulating long non‑coding RNA MIR100HG

Zhang,Guojun; Gao,Lei; Zhang,Junliang; Wang,Rui; Wei,Xiangdong

doi:10.3892/ol.2023.13917

Long non‑coding RNA PTCSC3 suppresses triple‑negative breast cancer by downregulating long non‑coding RNA MIR100HG

Authors:
- Guojun Zhang
- Lei Gao
- Junliang Zhang
- Rui Wang
- Xiangdong Wei
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Affiliations: Department of General Surgery, Changle People's Hospital, Changle County, Shandong 262499, P.R. China
Published online on: June 15, 2023 https://doi.org/10.3892/ol.2023.13917
Article Number: 331
Copyright: © Zhang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Long non‑coding RNA (lncRNA) PTCSC3 is characterized as a tumor suppressor in thyroid cancer and glioma. The present study aimed to investigate the role of PTCSC3 in triple‑negative breast cancer (TNBC). A total of 82 patients with TNBC were enrolled in the present study. The results showed that PTCSC3 was downregulated, while lncRNA MIR100HG was upregulated in tumor tissues compared with that in adjacent non‑cancerous tissues of patients with TNBC. The follow‑up study showed that low expression levels of PTCSC3 and high expression levels of MIR100HG were closely associated with poor survival of patients with TNBC. The expression levels of MIR100HG were decreased with the clinic stages of TNBC, while the expression levels of MIR100HG showed the opposite trend. Correlation analysis showed that the expression levels of PTCSC3 and MIR100HG were significantly correlated in both tumor tissues and adjacent non‑cancerous tissues. The overexpression of PTCSC3 inhibited the expression level of MIR100HG in TNBC cells, while the expression level of PTCSC3 was unaffected. Cell Counting Kit‑8 and Annexin V‑FITC Apoptosis flow cytometry assays showed that overexpression of PTCSC3 led to inhibition, while overexpression of MIR100HG led to the promotion of TNBC cells viability and inhibited apoptosis of TNBC cells. In addition, overexpression of MIR100HG attenuated the effects of PTCSC3 overexpression on cancer cell viability. However, the overexpression of PTCSC3 did not affect cancer cell migration and invasion. Western‑blot analysis showed that PTCSC3 suppressed viability and promoted apoptosis of TNBC cells through the Hippo signaling pathway. Thus, the present study demonstrated that lncRNA PTCSC3 inhibits cancer cell viability and promotes cancer cell apoptosis in TNBC by downregulating MIR100HG.

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