ETS1 expression

These preliminary findings correlate PARPi-induced oxidative DNA damage/oxidative stress to Ets-1 expression in breast cancer cells.

The identification of a novel microRNA involved in the anti-angiogenic mechanism in NPDR provides new insights into the molecular underpinnings of endothelial dysfunction in diabetic retinopathy. Our retina-specific circulating microRNA panel has potential utility in risk assessment and early detection of NPDR.

The in vivo study demonstrated that inhibition of LINC00887 suppressed CRC metastasis, but this inhibitory effect was nullified when mice were treated with NaCr. In conclusion, our results confirmed the diagnostic biomarker potential of H3K27cr in individuals with CRC, and proposed a functional model to elucidate the involvement of LINC00887 in promoting CRC metastasis by elevating H3K27cr level.

Downregulation of ETS1 expression correlated with poor prognosis and immune infiltration in ccRCC, further suggesting that ETS1 may be a biomarker for better prognosis in ccRCC patients.

Besides, MiR-579-3p also could relieve OGD/R-induced SK-N-SH cell apoptosis, inflammation and oxidative stress by targeting ETS1. Our findings indicated that circ_0059662 knockdown alleviated OGD/R-induced SK-N-SH cell injury by sponging miR-579-3p to regulate ETS1 expression.

Our animal studies showed that inhibition of MMP-2 and ETS-1 by genetic knockout improved AVF development. Therapeutic approaches of inhibiting these molecules may enhance AVF maturation in hemodialysis patients.

A high expression of ETS1 is associated with the progression of ccRCC. This study suggests that ETS1 promotes proliferation by increasing MMP2 expression in ccRCC, and combined knockdown of ETS1 and inhibition of ERK can significantly inhibit the proliferation, migration and invasion of ccRCC. ETS1 may be a therapeutic and prognostic target for renal cell carcinoma.

The herein reported data establish MYC as a key determinant of lineage commitment in PLC and provide a molecular explanation why common liver damaging risk factors such as alcoholic or non-alcoholic steatohepatitis can either lead to HCC or iCCA.

ETS1 positively regulates the expression of NDRG1 and promotes OSCC. Therefore, ETS1 may serve as a new target for the clinical diagnosis and treatment of OSCC.

Either administration or overexpression of the peptides harboring the interaction segment strongly inhibits the colony formation and migration of SW480 cells. Our findings suggest that the interaction between Ets1 and Sp1 rather than Ets1 alone promotes transformation in SW480 cells and provide new insight into the Ets1 and Sp1 interaction as an antitumour target in SW480 cells.

Our findings suggest for the first time that the 5-HT7 receptor promotes FOXM1, eEF2K and cyclin D1 signaling to support TNBC cell proliferation; thus, inhibition of 5-HT7 receptor/FOXM1 signaling may be used as a potential therapeutic strategy for targeting TNBC. 5-HT induces cell proliferation of TNBC cells through 5-HT7 receptor signaling. Also, genetic and pharmacological inhibition of 5-HT7 by RNAi (siRNA) and metergoline HTR7 antagonist, respectively inhibits FOXM1 oncogenic transcription factor and suppresses TNBC cell proliferation.