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

Sep 24, 2026

Uploaded by Jacob

Long non-coding RNA PTCSC3 functions as a tumor suppressor in thyroid cancer and glioma, prompting investigation of its role in triple-negative breast cancer (TNBC). Eighty-two TNBC patients were enrolled and PTCSC3 was downregulated while MIR100HG was upregulated in tumor tissue versus adjacent non-cancerous tissue. Low PTCSC3 and high MIR100HG expression correlated with poorer survival. PTCSC3 overexpression decreased MIR100HG and inhibited TNBC viability and promoted apoptosis, whereas MIR100HG overexpression counteracted PTCSC3 effects. PTCSC3 suppressed viability and promoted apoptosis via the Hippo signaling pathway.

LanguageEnglish

CategoryHealthcare

FormatPDF

Pages10

Reading Time25 min

AccessFree to download

Abstract

Introduction

Materials and methods

Research subjects

Specimens and cell lines

ONCOLOGY LETTERS 26: 331, 2023 Long non‑coding RNA PTCSC3 suppresses triple‑negative breast cancer by downregulating long non‑coding RNA MIR100HG GUOJUN ZHANG, LEI GAO, JUNLIANG ZHANG, RUI WANG and XIANGDONG WEI Department of General Surgery, Changle People's Hospital, Changle County, Shandong 262499, P.R. China Received December 19, 2018; Accepted September 13, 2021 DOI: 10. 3892/ol.2023.13917 Abstract. Long non‑coding RNA (lncRNA) PTCSC3 is char‑ acterized 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 inhib‑ ited 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 addi‑ tion, overexpression of MIR100HG attenuated the effects of PTCSC3 overexpression on cancer cell viability. However, the overexpression of PTCSC3 did not affect cancer cell migra‑ tion 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. Correspondence to: Dr Guojun Zhang, Department of General Surgery, Changle People's Hospital, 278 Limin Road, Changle County, Shandong 262499, P.R. China E‑mail: [2558486080@qq.com](2558486080@qq.com) Key words: triple‑negative breast cancer, long non‑coding RNA PTCSC3, long non‑coding RNA MIR100HG, viability, apoptosis Introduction The latest genome‑wide transcriptome analyses revealed that ~2/3 of the genomic DNA of mammalian species is transcribed but >98% of the transcripts lack protein‑coding capacity (1), indicating that most mammalian genes are non‑protein coding genes. Long non‑coding RNAs (lncRNAs) are a class of transcripts with pivotal biological functions in many processes (2), such as cell growth, embryonic develop‑ ment, and disease progression by regulating downstream genes at post‑transcriptional and translational levels (3,4) . Extensive studies have shown that lncRNAs play critical roles in cancer biology (5), and regulation of lncRNAs has shown potentials in inhibiting cancer development (6). However, functions of most lncRNAs are still unknown. Although the mortality rate of breast cancer has dropped significantly during the past decades, it still accounts for >1/5 deaths among females (7) . As a major subtype of breast cancer, triple‑negative breast cancer (TNBC) is characterized by inhibited expression of estrogen receptor α , progesterone receptor, and human epidermal growth factor receptor 2 (8). The development and progression of TNBC involve the regulation of multiple lncRNAs (9,10) . lncRNA PTCSC3 is characterized as a tumor suppressor in glioma and thyroid cancer, while its role in the recurrence of TNBC is unknown (11‑13) . It was reported that lncRNA MIR100HG promotes cell viability

FAQs

What was the main goal of the study on PTCSC3 in TNBC?

To determine the role of the lncRNA PTCSC3 in triple-negative breast cancer and assess its potential interaction with lncRNA MIR100HG.

How were PTCSC3 and MIR100HG expression levels different in TNBC tissues?

PTCSC3 was downregulated and MIR100HG was upregulated in TNBC tumor tissues compared with adjacent non-cancerous tissues.

What effects did PTCSC3 and MIR100HG overexpression have on TNBC cells?

Overexpression of PTCSC3 inhibited TNBC cell viability and promoted apoptosis; overexpression of MIR100HG promoted viability and inhibited apoptosis, and MIR100HG attenuated PTCSC3’s effects. PTCSC3 did not affect migration and invasion.

Sep 24, 2026

Uploaded by Jacob