QKI (QKI, KH Domain Containing RNA Binding)

Functional assays demonstrate that QKI overexpression in T-ALL cells significantly reduces cell proliferation, induces G0/G1 cell cycle arrest, and limits leukemia progression and dissemination, ultimately improving survival in xenograft models. Together, these findings provide compelling evidence that QKI functions as a regulator of RNA splicing with tumor-suppressive activity in T-ALL.

AGs are rare tumors with a higher tendency in males and they usually involved the frontal and temporal lobe. In immunohistochemical studies, GFAP and EMA are frequently positive. The MYB-QKI gene fusion is a characteristic feature of this tumor. GTR was regarded as the best treatment. Although most AGs were clinically indolent, a few unusual cases showed aggressive behaviors. A larger cohort with long-term follow-up is necessary to verify our findings.

However, the regulatory roles of QKI in EC biology remain poorly described. This review summarizes our current understanding of the QKI isoforms and their functions in ECs, as well as the potential utility of QKI as an emerging translational target for angiogenic-based therapies.

ROBO2 and GPR180/CG9304 were down and upregulated, respectively, in flies and patients with RAF fusions. Our study provides mechanistic insights into pLGG tumorigenesis and suggests targeting repulsive guidance signaling and GPR180/CG9304 as potential therapeutics for pLGG subtypes.

Reduced QKI expression has been documented in MS and its experimental models. In this context, this review summarizes current evidence positioning QKI as a central regulator of myelin maintenance and regeneration and highlights its potential as a therapeutic target for demyelinating diseases.

In summary, our study elucidates a critical circ_0001766/miR-1203/PPP1R3C axis that modulates CRC progression and rapamycin resistance. Our findings highlight circ_0001766 as a promising therapeutic target in CRC, providing a new avenue for enhancing the efficacy of existing treatments and overcoming drug resistance.

The hub SF MBNL1 identied in the present study could inhibit the progression of ccRCC. This effect is likely due to the regulation of QKI expression through AS.

Simultaneously, YY1 upregulates QKI expression, facilitating splicing events leading to the formation of hsa-circ-0000326. Inhibiting exosomal hsa-circ-0000326 presents a potential therapeutic approach for treating metastatic PCa.

QKI play a critical role as tumour suppressor or an oncogene in tumour progression due to the different splicing sites and transcripts with various tumour subtype or tumor micorenvironment. Ongoing research about QKI's functions and mechanisms persist is required to conduct for better understanding the role of QKI in tumour regulation.

Especially in Glioblastoma Multiforme (GBM), although QKI is not the primary mutation, it still plays a vital role in maintaining the stemness of GBM. However, the mechanisms and further studies on this topic demand extensive basic and clinical trials.

Notably, overexpression of long non-coding RNA eosinophil granule ontogeny transcript (EGOT) physically binds to QKI and suppressed its activity by inhibiting ubiquitin specific peptidase 25 (USP25) mediated deubiquitination and subsequent degradation of QKI. Collectively, these data demonstrate the novel mechanistic links between the splicing factor QKI and splicing event in PTC metastasis and support the potential utility of targeting splicing events as a therapeutic strategy for PTC.

High QKI expression was identified in HCCs and associated with poor RFS. QKI might be a prognostic biomarker of HCCs associated with epithelial-to-mesenchymal transition and a potential candidate therapeutic target.