Retracted: Long noncoding RNA TALNEC2 plays an oncogenic role in breast cancer by binding to EZH2 to target p57^KIP2 and involving in p‐p38 MAPK and NF‐κB pathways

Abstract

We aimed to investigate the potential role and regulatory mechanism of long noncoding RNA tumor‐associated lncRNA expressed in chromosome 2 (TALNEC2) in breast cancer. The expression of TALNEC2 in breast cancer tissues and cells were investigated. MCF‐7 and MDA‐MB‐231 cells were transfected with small interfering RNA (siRNA) duplexes for targeting TALNEC2 (si‐TALNEC2), enhancer of zeste homolog 2 (EZH2; si‐EZH2) and p57KIP2 (si‐p57 KIP2), and their corresponding controls (si‐NC). The viability, colony forming ability, cell cycle, apoptosis, and autophagy of transfected cells were assessed. The expressions of p‐p38 mitogen‐activated protein kinase (MAPK) and nuclear factor κB (NF‐κB) pathway‐related proteins were investigated. The results showed that TALNEC2 was highly expressed in breast cancer tissues and cells. Knockdown of TALNEC2 significantly inhibited the malignant behaviors of MCF‐7 and MDA‐MB‐231 cells, including inhibiting cell viability and colony forming, arresting cell cycle at G0/G1 phase, inducing cell apoptosis, and promoting cell autophagy. EZH2 was a TALNEC2 binding protein, which was upregulated in breast cancer tissues and cells and could negatively regulate p57 KIP2. Effects of TALNEC2 knockdown on malignant behaviors of MCF‐7 cells were reversed by p57 KIP2 knockdown. The expressions of p‐p38, RelA, and RelB in MCF‐7 cells were decreased after knockdown of TALNEC2 or EZH2, which were reversed by knockdown of p57 KIP2 concurrently. In conclusion, TALNEC2 may play an oncogenic role in breast cancer by binding to EZH2 to target p57 KIP2. Activation of p‐p38 MAPK and NF‐κB pathways may be key mechanisms mediating the oncogenic role of TALNEC2 in breast cancer. TALNEC2 may serve as a promising target in the therapy of breast cancer.

Long non-coding RNA-based signatures to improve prognostic prediction of breast cancer

“…[ 22 23 ] For BC, emerging investigations have emphasized the vital function of lncRNAs in tumorigenesis and development. [ 24 25 26 ] For example, UASR1 has a high expression in BC tissues and promotes cancer cell growth, proliferation, wound healing and migration through the AKT/mTOR signaling pathway. [27] MALAT1 is considered an oncogenic regulator of BC, which accelerates angiogenesis through miR-145 in MCF-7 cells to enhance aggressiveness of BC.…”

Oncogenic seRNA functional activation: a novel mechanism of tumorigenesis

“…The two signaling pathways synergistically accelerate autophagy and strengthen oncogenic activity of SCC [80,81]. In addition, the enhancer of zeste homolog 2 (EZH2) mediates p38 MAPK activation via directly binding with seRNA, and the activated EZH2 induces autophagy through promoting p38 MAPK phosphorylation, following the upregulated autophagy genes including Agt5 and LC-3II [108,109] ( Fig. 5).…”

lncRNA SNHG3 promotes breast cancer�progression by acting as a miR‑326 sponge

“…For example, Zhang et al revealed that lncRNA MEG3 inhibits breast cancer progression partially via the activation of the endoplasmic reticulum (ER) stress, NF-κB and p53 pathways (13). Qiao et al revealed that TALNEC2 functions as a breast cancer oncogene in order to target p57 KIP2 by binding to EZH2 via the p-p38 MAPK and NF-κB pathways (14). Kong et al found that lncRNA-CDC6 acts as a competing endogenous RNA (ceRNA) that sponges miR-215 to single out CDC6 resulting in enhancement of breast cancer progression and stage (15).…”