Retracted: Inhibitory role of large intergenic noncoding RNA‐ROR on tamoxifen resistance in the endocrine therapy of breast cancer by regulating the PI3K/Akt/mTOR signaling pathway

Abstract

Breast cancer (BC) is the second-leading cause of central nervous system metastases among severe malignancies. This study aimed at investigating the underlying mechanism by which large intergenic noncoding RNA-regulator of reprogramming (lincRNA-ROR) affects the tamoxifen (TAM) resistance of BC cells by regulating the PI3K/Akt/mTOR signaling pathway. Immortalized human mammary epithelial cell line (MCF10A) and BC cell lines (MCF-7, MDA-MB-231, T47D, BCAP-37, and ZK-75-1) were cultured, and BC tissues and adjacent normal breast tissues were collected from 152 BC patients. LincRNA-ROR expression in tissues and cells were detected using reverse transcription quantitative polymerase chain reaction. RNA interference was used to silence lincRNA-ROR in MDA-MB-231 cells, and then the cell proliferation and apoptosis were detected by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and annexin-V and propidium iodide (PI) double staining respectively. The expression of apoptosis-related proteins and PI3K/Akt/mTOR signaling pathway-related proteins was measured by performing western blot assay. The BC tissues and cells presented a higher expression of lincRNA-ROR. MAD-MB-231 cells exhibited the highest lincRNA-ROR expression. After lincRNA-ROR silencing, MAD-MB-231 cells showed decreased proliferation, and increased sensitivity to TAM. Besides, the apoptosis-promoting effect of TAM on MAN-MB-231 cells significantly increased. The expression of PI3K/Akt/mTOR signaling pathway-related proteins and the PI3K/Akt/mTOR signaling pathway were repressed by TAM after silencing lincRNA-ROR. Our study demonstrated that silencing lincRNA-ROR could increase the sensitivity of BC MAD-MB-231 cells to TAM by suppressing the activation of P13K/Akt/mTOR signaling pathway.

Long non-coding RNAs: Functional regulatory players in breast cancer

“…RoR is ∼2.6 kbp and is located on 18q21.31. RoR is an oncogenic lincRNA that is highly expressed in self-renewing human embryonic stem cells and various cancer cells such as hepatocellular carcinoma [93], endometrial cancer [94], pancreatic cancer [95] and BC [[96], [97], [98]]. In several contexts, there is a positive correlation between the expression level of RoR and the undifferentiation degree of the carcinoma tissues [99].…”

Tenacissoside H Induces Apoptosis and Inhibits Migration of Colon Cancer Cells by Downregulating Expression of GOLPH3 Gene

“…We found that TDH had a significant concentration-dependent inhibitory Evidence-Based Complementary and Alternative Medicine effect on the proliferation of human colon cancer LoVo cells in vitro; moreover, it can also induce apoptosis and inhibit the migration of LoVo cells; these results indicated that TDH could inhibit colon cancer cell viability and metastasis. e abnormal activation of the PI3K/AKT/mTOR signaling pathway has been observed in a variety of human tumors, including esophageal, ovarian, breast, and colorectal cancer and promoted the development of tumor by promoting cell proliferation, inhibiting apoptosis, or activating angiogenesis [16][17][18][19]. e aberrant activation of the Wnt/β-catenin signaling pathway has been also demonstrated in colorectal cancer and regulates gene expression and cell invasion, migration, proliferation, and differentiation in the initiation and progression of CRC [20].…”

Long Non-Coding RNA in the Pathogenesis of Cancers

“…In TNBC tissues [202,203] and cell lines [201,202,203], the level of lincRNA-ROR is increased. Overexpression of lincRNA-ROR in TNBC cell line MDA-MB-231 promotes cell invasion and metastasis, while inhibition of lincRNA-ROR expression exerts the opposite effects [202,204].…”