ILK (Integrin Linked Kinase)

The resulting reduction in NHE1-/ILK-dependent migration and ATP production is rescued by hypoxia across cell types. While certain cancer cells can adapt to long-term (>3 weeks) acidosis and acquire an aggressive phenotype, acidosis-induced adaptation is not universal and depends on the cell's ability to restrain reactive oxygen species overproduction via fatty acid oxidation.

The area under the curve for ILK was calculated to be 0.687 (95% CI: 0.600-0.773), while for FABP4, it was 0.638 (95% CI: 0.548-0.728). The current research demonstrates that the positive expression of ILK and FABP4 is significantly linked to the pathogenesis, clinical manifestations, pathological characteristics, biological behaviors, and unfavorable prognosis in EHCC.

S100A4 may contribute to this mechanism by modulating Snail protein. These findings imply that simultaneously targeting both ILK and S100A4 represents a novel and promising therapeutic strategy to suppress SACC progression.

Most ITF signals are likely contaminants. We identified N. crassa as associated with unfavorable prognosis in OvCa, potentially via modulation of the extracellular matrix.

Our results indicate that high ILK expression is associated with EMT in LUAD patients and that genetic suppression of ILK can limit EMT progression and reduce the viability of DTP cells by impairing YAP activation, ultimately improving osimertinib (Osi) sensitivity in LUAD cells...Lastly, we found that strong immunohistochemistry staining of ILK in patient biopsies was significantly associated with and may be used to predict receptor tyrosine kinase-independent mechanisms of EGFR-TKI resistance. Overall, our results suggest that ILK is an important regulator of EGFR-TKI response and may be exploited as a predictor for acquired resistance, providing evidence for co-targeting ILK with EGFR to better control minimal residual disease and EGFR-TKI resistance in lung cancer.

Thus, our results suggest that hypoxia induced an increase in MiR-542-3p expression, which caused an increase in binding to ILK gene and negatively regulated ILK expression. This in turn, caused a decrease in Myocardin expression leading to phenotypic transition, proliferation, and increased migration of PASMCs, causing hypoxic pulmonary vascular remodeling and ultimately leading to HPH.

The ILK is an oncogene mainly through influencing the C-MYC in PCa. Inhibition of ILK expression would be a promising method for treating the development and progression of PCa.

Our data revealed that platelet-related indices were abnormally ascendant in iCCA patients compared to healthy adults. Co-culturing with platelets enhanced the progression of EMT, and the motility and viability of iCCA cells in vitro and in vivo. Proteomic profiling discovered that platelets promoted the development of iCCA through FAK/PI3K/AKT pathway by means of elevating the expression of ILK and ITGB3, indicating that both proteins are promising therapeutic targets for iCCA with the guidance of platelet-related indices.

ILK showed no prognostic value. Further studies with larger cohorts are needed to identify prognostic and predictive biomarkers facilitating optimized individual treatment decision in this rare type of cancer.

RNF19A suppressed the proliferation, migration, and invasion abilities of BCa cells by regulating ILK ubiquitination and inactivating the AKT/mTOR signalling pathway. RNF19A might be a potential prognostic biomarker and promising therapeutic target for BCa.

These results indicated that the higher potential of metastatic tumor cells in vascular-like structure formation may be related to higher expression of ILK and FAK. Analysis of molecular features of metastatic tumor cells could be utilized to create a targeted therapeutic strategy against metastasis in breast cancer.

Finally, we find that ILK expression correlates with expression of STAT3-regulated proteins and protein signatures describing astrocyte-like and mesenchymal states in patient tumors. This work identifies ILK as a pivotal regulator of multiple malignancy-associated GBM phenotypes, including phenotypic plasticity and mesenchymal state.