IncRNA TYMSOS Promotes Epithelial-Mesenchymal Transition and Metastasis in Thyroid Carcinoma through Regulating MARCKSL1 and Activating the PI3K/Akt Signaling Pathway

LncRNA TYMSOS facilitates breast cancer metastasis and immune escape through downregulating ULBP3

“… 7 In addition, lack of TYMSOS suppresses cell growth, migration, invasion, epithelial-mesenchymal transition, or self-renewal capabilities of various cancer cells. 6 , 7 , 9 , 10 More importantly, TCGA data support that TYMSOS is upregulated in breast cancer, and it has been identified as a risk lncRNA in breast cancer. 21 In accordance with these reports, we found that TYMSOS was markedly increased in breast tumors, especially metastatic breast tumors.…”

“…In the past decade, emerging evidence illustrates that TYMSOS functions as an oncogene in different cancers, including GC, NSCLC, thyroid carcinoma, and osteosarcoma. 6 , 7 , 8 , 9 , 10 Several TYMSOS-associated competing endogenous networks have been identified. For instance, FOXM1/TYMSOS/miR-214-3p/NCAPG axis facilitates NSCLC progression by modulating cell proliferation, stemness, migration, and immune cell infiltration.…”

“… 5 Aberrant expression of thymidylate synthetase opposite strand (TYMSOS) has been observed in different cancers. 6 , 7 , 8 , 9 , 10 For instance, TYMSOS promotes cell proliferation, migration, and invasion in gastric cancer (GC) through miR-4739/ZNF703 axis. 6 It is also identified as an oncogene in non-small-cell lung cancer (NSCLC), thyroid carcinoma, and osteosarcoma.…”

“… 6 It is also identified as an oncogene in non-small-cell lung cancer (NSCLC), thyroid carcinoma, and osteosarcoma. 7 , 8 , 9 , 10 Notably, The Cancer Genome Atlas (TCGA) data indicate that TYMSOS is elevated in breast cancer. However, the biological role of TYMSOS on immune escape in breast cancer remains ambiguous.…”

The lncRNA HOTAIR: a pleiotropic regulator of epithelial cell plasticity

“…Of note, also in gallbladder cancer the oncogenic activity of HOTAIR in promoting invasion and malignancy of tumor cells has been ascribed, at least in part, to its-mediated negative regulation of miR-130a [ 19 ]. Notably, this miRNA was also proven to counteract the invasive and metastatic potential of NSCLC cells by interfering with the expression of the transcription factor Runx2 [ 88 ]; conversely, its inhibition can be enforced by the lncRNA TYMSOS to promote EMT in thyroid cancer cells [ 89 ]. Notably, in colorectal cancer, HOTAIR-mediated modulation of ZEB1 expression was further ascribed to the negative regulation of miR-1277-5p [ 90 ].…”