RUNX1 overexpression

RUNX family genes were abnormally expressed in KIRC patients, and were closely related to the crosstalk of immune cells. Our findings may help to understand the pathogenesis and immunologic roles of the RUNX family in KIRC patients from new perspectives.

Overexpressing RUNX1 antagonized the suppression of RIPK4 knockdown on RUNX1, Wnt3a, p-GSK-3β, cytoplasmic β-catenin, nuclear β-catenin, Cyclin D1, CDK4, Cyclin E, and c-Myc levels. Collectively, miR-575/RIPK4 axis repressed COAD progression via inactivating the Wnt/β-catenin pathway through downregulating RUNX1.

In addition, miR-429 mimic significantly suppressed tumor growth, inflammatory cell infiltration, EMT, and ITGB1 expression in vivo, which were inhibited by RUNX1 overexpression. Altogether, these results indicate that the RUNX1/miR-429 feedback loop promoted growth, metastasis, and EMT in OSCC by targeting ITGB1.

This study evaluated the differences between the MLL, RUNX1, and inv(16) AML subtypes at the single-cell level, discovered gene signatures that effectively discriminate between the three subtypes as well as other AML and healthy samples, and revealed that the poorer prognosis of the MLL subtype may be attributable to dysregulation of CD8+ T-cell proliferation caused by abnormalities in the SPI-B TF and the LCK signaling pathway.

RUNX1 is a poor prognostic factor of clear cell renal carcinoma, which may provide a novel therapeutic target for ccRCC.

In vitro experiments, we found that RUNX1 overexpression promoted cell proliferation and migration functions and affected downstream functional proteins by regulating the activity of the mTOR pathway, as confirmed by an analysis using the mTOR pathway inhibitor rapamycin. In addition, RUNX1 affected PD-L1 expression via the mTOR pathway. These results indicate that RUNX1 is a potential therapeutic target for NSCLC.

Taken together these data underline the complexity of the mechanisms involved in venetoclax resistance and showed that the loss of BCL2 dependency can be due to NOXA downregulation and upregulation of MCL-1 and RUNX-1. Therefore, the use of agents that can prime BCL2-dependency through upregulation of NOXA and shifting BIM loading to BCL2 (RUNX1 inhibitors) could be explored in combination with venetoclax in MM patients who acquire MCL1 dependence following treatment.

Our concise review on the emerging RUNX1 roles in different tissues outside the hematopoietic context provides a number of well-funded hypotheses that will open new research avenues toward a better understanding of RUNX1-mediated transcription in health and disease, contributing to novel potential diagnostic and therapeutic strategies for Down syndrome-associated conditions.

Our data suggest a combined impact of the ETV6::RUNX1 fusion protein and RNA binding protein, IGF2BP1 in activating multiple oncogenic pathways in B-ALL which makes IGF2BP1 and these pathways as attractive therapeutic targets and biomarkers.

A decreasing metastasis of both HA-treated cell lines was evidenced through a downregulation of MMP2 and MMP9 via the Akt/P38/JNK-MAPK signaling pathway. Overall, our approach first demonstrated that RUNX1 enhanced EMT-driven prostate cancer metastasis and that HA was capable of inhibiting the EMT and metastatic processes and should probably be considered as a candidate for metastasis PCa treatment.

RUNX1-IT1 may suppress the GC cell movement by inhibiting the maturation of miR-20a.

RUNX1 was highly expressed in cervical cancer, and upregulated RUNX1 could significantly promote the invasive abilities of cervical cancer cells by inducing EMT. Therefore, RUNX1 may be a potential biomarker for early diagnosis and targeted therapy of cervical cancer.

These findings indicate that the Runx1-mediated P2X3R gene transcription resulted from activation of GDNF-GFRα1-Ret-ERK signaling contributes to the sensitization of DRG neurons and pathogenesis of bone cancer pain. Our findings identify a potentially targetable mechanism that may cause bone metastasis-associated pain in cancer patients.

Obtained results should be interpreted with caution. Further analysis in this research field is needed.

To conclude, the present study provided a novel mechanism, whereby TRAIL is a target gene of RUNX1 and TRAIL expression was inhibited by RUNX1‑ETO. These results suggest that TRAIL is a promising agent for the clinical treatment of t(8;21) AML.

Together, the present study indicates that RUNX1 confers TMZ resistance in GBM by upregulating MRP1, which is negatively regulated by miR-128-3p. Targeting miR-128-3p/RUNX1/MRP1 axis provides a potential strategy to overcome TMZ resistance in GBM.

Additionally, the overexpression or knockdown of lncRNA RUNX1-IT1 regulated the invasion ability of cells by affecting expressions of E-cadherin, N-cadherin, and Vimentin. The poor expression, overexpression, or knockdown of lncRNA RUNX1-IT1 affects the stemness and invasion ability of lung cancer cells.

Importantly, RUNX1 knockdown impaired the metastatic capability of colorectal cancer cells in vivo and induced the development of angiogenic lesions in liver. Our results confirm that RUNX1 may be a potential target to overcome vessel co-option in CRCLM.

miR-27b-3p was down-regulated in GC, and it could regulate the Hippo pathway and affect EMT by inhibiting RUNX1 expression.

Circ_0027599 overexpression repressed GC progression via modulation of miR-21-5p/RUNX1 axis, which might illumine a novel therapeutic target for GC.

In addition, RUNX1-IT1 overexpression reduced the effects of miR-195 overexpression on cell proliferation. RUNX1-IT1 may sponge miR-195 to upregulate cyclin D1, thereby increasing the proliferation of glioblastoma cells.

Overexpression of RUNX1-IT1 suppressed the role of miR-21 in increasing cell proliferation. RUNX1-IT1 is downregulated in EC and inhibits cancer cell proliferation by suppressing the maturation of miR-21.

Here, we report that RUNX1, expressed highly in DRG, binds HSV-1 genome, represses transcription of numerous viral genes, and suppresses productive in vitro infection. Our computational work further suggests this strategy may be employed by other herpesviruses to reinforce latency in a cell-specific manner.