PFN1 (Profilin 1)

Finally, we demonstrate that Pfn1 inhibitor is amenable to lipid microbubble encapsulation and release in the tumor microenvironment (TME) by ultrasound-mediated disruption of circulating microbubbles to achieve anti-angiogenic and anti-tumor benefit. In summary, our findings suggest that tumor-localized release of Pfn1 inhibitor could be a potential therapeutic strategy in RCC.

Our findings revealed that nuclear Pfn1 acts as a tumor suppressor by inhibiting DNA replication and cell growth, while cytoplasmic Pfn1 promotes tumorigenesis by enhancing stemness and replication efficiency. These results highlight the dual role of Pfn1 in breast cancer progression, governed by its subcellular localization. They suggested that modulating Pfn1 nuclear-cytoplasmic shuttling may be a potential therapeutic strategy.

The integration of FTIR spectroscopy into this study highlights the potential of infrared spectroscopy as a powerful tool in cancer research. These findings demonstrate that targeting critical regulatory pathways induces cytoskeletal and biochemical remodelling in melanoma CSCs, offering a multi-dimensional perspective on cellular plasticity.

Finally, we undertook a chemical optimization approach to design and synthesize 4,4'-((4- (trifluoromethyl)phenyl)methylene)bis(3,5-dimethyl-1 H -pyrazole), a structural analog of our originally identified inhibitor, that exhibits improved anti-angiogenic efficacy. In summary, our findings suggest that tumor-localized release of Pfn1 inhibitor could be a potential therapeutic strategy in RCC.

The observation of recurrent mutations highlights the causative role of PFN1 (L112P) in early-onset PDB/GCT within the Chinese population and provides insights into the physio-pathological functions of Profilin 1.

These results indicated that CD138 plays an important role in the resistance of MM cells to bortezomib. Targeting PFN1, CD138, or autophagic pathways may provide a promising therapeutic strategy for overcoming PFN1-induced drug resistance in MM.

Interestingly, the effect of circ_0000972 overexpression on such progresses was reversed by PFN1 silencing. This study elucidates that circ_0000972, an antitumor factor, sponges miR-96-5p to inhibit oncogenic cellular process in HCC by mediating PFN1 expression.

This model effectively forecasts responses to both immune therapy and chemotherapy. By regulating the immune microenvironment and targeting the key gene PFN1, it may improve the prognosis for high-risk patients.

Moreover, PFN1 knockdown exacerbated the mitophagy in LUAD cells and mitophagy inhibitor mitochondrial division inhibitor 1 (Mdivi-1) notably reversed the effects of PFN1 down-regulation on the proliferation, apoptosis as well as macrophage polarization in LUAD cells. To sum up, activation of mitophagy initiated by PFN1 depletion might obstruct the occurrence and M2 macrophage polarization in LUAD.

Here, we will review these newly discovered roles for PFN1, speculate on their contribution to ALS, and discuss how defects in actin can contribute to these processes. By understanding profilin 1's involvement in ALS pathogenesis, we hope to gain insight into this functionally complex protein with significant influence over cellular physiology.

Additionally, the hub gene PFN1 is highly expressed in MM, knocking down PFN1 induces cell cycle arrest, suppresses cell proliferation and promotes cell apoptosis. In conclusion, our study revealed that LRGs signature is a promising biomarker for MM that can effectively early distinguish high-risk patients and predict prognosis.

The positive expression rates of Ki-67 and PFN1 in bladder tumor tissue are significantly higher than those in bladder tissue, and pathological pattern, histological grade, clinical stage, infiltration, and lymph node metastasis are related to the positive expression rates of Ki-67 and PFN1, and different genders, ages, tumors diameter and vascular invasion are not related to the positive expression rates of Ki-67 and PFN1. The survival time and three-year survival rates of bladder cancer patients with Ki-67 positive and PFN1 positive expression are shorter.