PXN (Paxillin)

Overall, these channels appear to have opposite role at the plasma membrane and intracellularly, since both the reduction of BK channel activity at the plasma membrane (either by decreased expression or by paxilline blockade) and the increased intracellular expression of this protein favor TNBC malignancy. Our findings suggest that BK channels may have multiple physiological implications in TNBC, depending on their function and the cellular organelle in which they are expressed.

These results suggest that nesfatin-1 promotes proliferation and migration in normal lung epithelial cells but not in lung cancer cells. Further research is needed to elucidate the molecular mechanisms underlying the differential effects of nesfatin-1 on normal and cancerous lung cells.

The expression level of MBNL3 and lncRNA PXN-AS1-L can predict gastric cancer mortality. Higher expression of MBNL3 and PXN was linked to aggressive gastric cancer and low overall and progression-free survival rates.

Based on multiple RNA-seq data of tissues and plasma exosomes, we identified PXN-AS1, RAD9A, SLC17A9 as diagnostic biomarkers for CHB detection. The model based on three biomarkers showed potential diagnostic value for detecting CHB. Additional validation with a larger sample size is essential to thoroughly assess the reliability of these three biomarkers and the model's performance.

Additionally, a significant promotion of cellular apoptosis and expression of apoptotic proteins when treatment with chloroquine (CQ)/rapamycin (Rapa). Meanwhile, when combined with paxilline, it was found that paxilline may have a synergistic effects with Rapa, jointly promoting cellular apoptosis and the expression of proapoptotic proteins. In conclusion, these findings reveled paxilline alleviates HCC through autophagy-mediated apoptosis.

Paxillin can be considered a reliable biomarker for identifying and comparing OPMDs and OSCC cancerous changes.

Our study suggests that RCC shows immunohistochemical expression of FAK, Src and paxillin proteins, and this expression varies in relation to the histologic type, the stage and the stage/grade/gender, respectively. These findings imply a possible involvement of the FAK/Src signalling pathway in the pathogenesis and progression of cancer in RCC, providing future perspectives for targeted therapies with inhibitors.

In conclusion, this study shows that YHB inhibits the PDGF-induced proliferation and migration of VSMCs by regulating the transcription factor FOXO3a and the mTOR/p38/FAK signaling pathway. Therefore, YHB may be a potential therapeutic candidate for preventing and treating cardiovascular diseases such as atherosclerosis and vascular restenosis.

However, there was not statistical difference of PXN protein expression between DC and OKC (p Value = 0.51) and unicystic and solid ameloblastoma (p = 0.58), also the same was true for cysts and tumors (p = 0.37). The expression of PXN is not related to the biological behaviors of odontogenic lesions.

Western blotting confirmed biotinylation and enrichment of FAK and vinculin, known interactors of Hic-5 and paxillin, as well as several potentially unique proximity interactors of Hic-5 and paxillin, including septin 7 and ponsin, respectively. Further investigation into the functional relationship between the unique interactors and Hic-5 or paxillin may yield novel insights into their distinct roles in cell migration.

Paxillin-knockout GCs from mice with DHT-induced PCOS also produced more estradiol than GCs from littermate controls. Thus, paxillin may be a novel target in the management of androgen-related disorders in women, such as PCOS.

Lutein can inhibit cell adhesion, reduce the expressions of MMPs, and suppress cell invasion and migration by inhibiting the process of epithelial-mesenchymal transition.