Human disease-related long noncoding RNAs: Impact of ginsenosides.

Ginsenosides in ginseng are known for their potential health benefits, including antioxidant properties and their potential to exhibit anticancer effects. Besides a various range of coding genes, ginsenosides impose their efficacy by targeting noncoding RNAs. Long noncoding RNA ( lncRNA) has gained significant attention from both basic and clinical oncology fields due to its involvement in various cancer cell activities such as proliferation, apoptosis, metastasis, and autophagy.

ELOVL2-AS1 suppresses tamoxifen resistance by sponging miR-1233-3p in breast cancer.

Tamoxifen (Tam) has long been a top treatment option for breast cancer patients, but the challenge of eliminating cancer recurrence remains. Here, we identify a signalling pathway involving ELOVL2, ELOVL2-AS1, and miR-1233-3p, which contributes to drug resistance in Tam-resistant (TamR) breast cancer. ELOVL2-AS1, a long noncoding RNA, was significantly upregulated by its antisense gene, ELOVL2, which is known to be downregulated in TamR cells.

Ginsenoside Rh2 Regulates the CFAP20DC-AS1/MicroRNA-3614-3p/BBX and TNFAIP3 Axis to Induce Apoptosis in Breast Cancer Cells.

While a number of coding genes have explained the anticancer activity of ginsenoside Rh2, little is known about noncoding RNAs. This study was performed to elucidate the regulatory activity of long noncoding RNA (lncRNA) CFAP20DC-AS1, which is known to be downregulated by Rh2. MiR-3614-3p, which potentially binds CFAP20DC-AS1, was screened using the LncBase Predicted program, and the binding was verified by assaying the luciferase activity of a luciferase/lncRNA recombinant plasmid construct.

Matrix Metalloproteinase-1 (MMP1) Upregulation through Promoter Hypomethylation Enhances Tamoxifen Resistance in Breast Cancer.

Background: Tamoxifen (tam) is widely used to treat estrogen-positive breast cancer. However, cancer recurrence after chemotherapy remains a major obstacle to achieve good patient prognoses. In this study, we aimed to identify genes responsible for epigenetic regulation of tam resistance in breast cancer.