FLNA (Filamin A)

In conclusion, our results suggest that FLNA may be associated with tumor invasiveness in GH-secreting pituitary tumors. While data on Pasireotide-treated patients are exploratory, further studies are needed to assess FLNA's potential as a treatment response marker in acromegaly.

These findings suggest that amplification and overexpression of FLNA could serve as a potential prognostic biomarker in HNSCC.

We therefore studied isolated human granulosa cells and granulosa tumor cells. We examined how filamin A is regulated and found that filamin A has specific roles in granulosa cell maturation and initiation of their hormone-producing function.

Furthermore, CACNA2D3 gene expression was increased after 5-AZA treatment in two cell lines, while FLNA gene showed fluctuations in its expression, suggesting that additional factors regulate FLNA expression, which could be related to tumor size, histology, ER, and PR. In conclusion, DNA methylation could be a regulatory factor for CACNA2D3 and its high expression was linked to clinicopathological characteristics of breast cancer patients, especially with a good prognosis.

Treatment of HCT116 cells with 20 μM DCPIB resulted in the reorganization and dispersion of aggregated FLNA proteins, coinciding with a notable reduction in the concentrations of DAG and PKC. In summary, LRRC8A modulates FLNA to influence cellular growth and migration through the DAG-PKC signaling pathway, and their combination could signify a prospective biomarker for colon cancer.

The LARP4-binding site on FLNA overlaps with the β-integrin tail-binding region, and in vitro assays revealed that LARP4 can compete with integrin β7 tails for FLNA R21 binding. These results suggest that the LARP4-FLNA interaction may regulate cell migration, at least in part, by competing with integrin tails, although this mechanism has yet to be confirmed in vivo.

Taken together, our study revealed multiple exosomal proteins which could be applied as candidate biomarkers in diagnosis of lung cancer.

In addition, an AUC of 0.595 was found when the metastatic group was distinguished from the non-metastatic group using the relative quantitative results of FLNA, and it seemed that the high-FLNA-expression group had a poorer long-term survival rate than the low-expression group. These findings suggested that high expression of FLNA in TEPs may indicate the incidence and metastasis of NSCLC and serve as a biomarker for high-risk estimation for NSCLC.

The results demonstrated that low-frequency rTMS could be a potential treatment for GBM, achieved by downregulating FLNA and FLNC expression. This study sheds light on the potential for rTMS as a therapeutic strategy for glioblastoma as well as other types of cancers.

Due to the relevance of SOCE in cell physiology, our results provide evidence of a novel mechanism for the regulation of Ca2+ influx with relevant pathophysiological implications.NOTE & NOTEWORTHY FLNA cleaving by calpain has been observed in a variety of tumoral, including prostate and colorectal cancer cells, as well as in nontumoral cells, leading to a C-terminal fragment encompassing repeats 16-24. Expression of the FLNA16-24 fragment in HEK-293 cells enhances Orai1 and STIM1 expression, as well as SOCE, a mechanism mediated by attenuation of Orai1α and STIM1 degradation, providing evidence for a novel mechanism for the regulation of SOCE in normal and malignant cells.

Patients with invasive micropapillary carcinoma generally have a better prognosis than those with invasive ductal carcinoma does, which could be attributed to the lower expression of pro-oncogenic genes in the former group; however, the underlying mechanism needs further investigation.

This study explored Wee1 expression in ACC and its regulation by FLNA, the effects of Wee1 inhibitor AZD1775, and the impact of FLNA on its efficacy in ACC cell lines and primary cells...In conclusion, we demonstrated that FLNA regulates Wee1 expression by promoting its degradation, suggesting that low FLNA typical of ACC leads to increased Wee1 with consequent cancer cells growth. It proposes Wee1 inhibition as a new potential therapeutic approach for ACC, particularly for those lacking FLNA.