Cell Adhesion & Migration最新文献

Background: Research on the function of HGH1 in breast cancer remains lacking.

Methods: TCGAand GEO (GSE45827) datasets investigated discrepancies in HGH1 expression in BC. An aggregate of 106 clinical samples were gathered through immunohistochemistry, KM curves were drawn for prognostic analysis, and the function of HGH1 of BC was predicted. Finally, the effects of HGH1 knockdown on MDA-MB-231 and MCF-7 BC cells were verified via CCK8, invasion, wound healing and colony formation assays.

Results: HGH1 is highly expressed in BC and is linked to unfavorable prognosis. HGH1 overexpression is connected to keratinization and the cell cycle and is closely related to ER and PR expression and tumor stage in BC patients. Knocking down HGH1 in BC cells inhibited the viability, invasion and migration.

Conclusion: Knockdown of HGH1 in breast cancer cell lines can inhibit the viability, invasion and migration of tumor cells.

The research endeavors to expound the role of ORM1 in bladder cancer (BCa) and the implied response mechanism. RT-qPCR and Western blotting examined ORM1 and S100A12 expression. Functional experiments assessed the cellular phenotypes. HDOCK and Co-IP confirmed the interaction of ORM1 and S100A12. Western blotting tested apoptosis- and ERK signaling-associated proteins. ORM1 and S100A12 were abundant in the BCa cells. ORM1 or S100A12 loss impaired cell proliferation, migration, and invasion, and aggravated cell apoptosis. ORM1 interacted with S100A12. ORM1 knockdown down-regulated S100A12 expression and inactivated ERK signaling.S100A12 overexpression or ERK activator reversed the impacts of ORM1 interference on ERK signaling and BCa cells. ORM1 mightdrive BCa via binding to S100A12 and activating ERK signaling.

This research aims to study the effect of magnetic nanoparticles of Fe3O4 (MNP Fe3O4) containing gambogic acid (GA-MNP Fe3O4) on colorectal cancer (CRC). MNP Fe3O4 enhanced the antitumor effect of GA by inhibiting the malignant behavior of CRC cells. RORB was a target of GA, and GA activated RORB expression to inhibit metastasis of CRC. Knockdown of RORB impaired the effect of GA-MNP Fe3O4 on CRC metastasis. EMILIN1 was a target of RORB, and RORB promoted transcription of EMILIN1. Overexpression of EMILIN1 reversed the effect of knockdown of RORB on GA-MNP Fe3O4 and inhibited metastasis in CRC. These findings revealed that MNP Fe3O4 enhanced the antitumor effect of GA and activated RORB to promote EMILIN1 transcription and inhibit CRC metastasis.

In this research, we investigated the role of PIK3R6, a regulatory subunit of PI3Kγ, known for its tumor-promoting properties, in clear cell renal cell carcinoma (CCRCC). Utilizing the UALCAN website, we found PIK3R6 upregulated in CCRCC, correlating with lower survival rates. We compared PIK3R6 expression in CCRCC tumor tissues and adjacent normal tissues using immunohistochemistry. Post RNA interference-induced knockdown of PIK3R6 in 786-O and ACHN cell lines, we performed CCK-8, colony formation, Edu staining, flow cytometry, wound healing, and transwell assays. Results showed that PIK3R6 silencing reduced cell proliferation, migration, and invasion, and induced G0/G1 phase arrest and apoptosis. Molecular analysis revealed decreased CDK4, Cyclin D1, N-cadherin, Vimentin, Bcl-2, p-PI3K and p-AKT, with increased cleaved caspase-3, Bax, and E-cadherin levels in CCRCC cells. Moreover, inhibiting PIK3R6 hindered tumor growth. These findings suggest a significant role for PIK3R6 in CCRCC cell proliferation and metastasis, presenting it as a potential therapeutic target.

The intensive study and investigation of neuroprotective therapy for central nervous system (CNS) diseases is ongoing. Due to shared mechanisms of neurodegeneration, a neuroprotective approach might offer benefits across multiple neurological disorders, despite variations in symptoms or injuries. C-Jun N-terminal Kinase 3 (JNK3) is found primarily in the CNS and is involved in physiological processes such as brain development, synapse formation, and memory formation. The potential of JNK3 as a target for pharmacological development holds promise for advancing neuroprotective therapies. Developing small molecule JNK3 inhibitors into drugs with neuroprotective qualities could facilitate neuronal restoration and self-repair. This review focuses on elucidating key neuroprotective mechanisms, exploring the interplay between neurodegenerative diseases and neuroprotection, and discussing advancements in JNK3 inhibitor drug development.

The potential of adult adipose-derived stromal cells (ADSCs) to differentiate into astrocytes holds promise for future cell transplantation therapies. However, the growth of differentiated astrocytes is unstable, and their survival rate is low. Endoplasmic reticulum (ER) pathway mediated apoptosis is one of the causes of cell death, but whether there is ER stress response in the differentiation of ADSCs into astrocytes is still unclear. In this study, the expression of protein factors related to endoplasmic reticulum stress (ERS) and apoptosis, including GRP78, ATF6, PERK, CHOP, Caspase12, and Caspase3, was detected in cells. It was found that the expression of ERS pro-survival factors was highest in the ADSCs group and decreased with prolonged induction time. Conversely, the expression levels of pro-apoptotic factors increased with the extension of induction time. Thus, ERS occurs during the differentiation of ADSCs into astrocytes, and ERS can mediate apoptosis of ADSC-derived astrocytes.

In September 2023 members of the cell adhesion and cell migration research community came together to share their latest research and consider how our work might be translated for clinical practice. Alongside invited speakers, selected speakers and poster presentations, the meeting also included a round table discussion of how we might overcome the challenges associated with research translation. This meeting report seeks to highlight the key outcomes of that discussion and spark interest in the cell adhesions and cell migration research community to cross the perceived valley of death and translate our work into therapeutic benefit.

Daphnetin, a coumarin derivative isolated from Daphne odorifera, has anti-tumor effects. The MAPK, STAT3, and NF-κB signaling pathways are closely related to the pathogenesis of lung cancer. To investigate the effect of daphnetin on anti-lung adenocarcinoma A549 cells and its mechanism. The anti-tumor effects of daphnetin on the proliferation, clone formation, migration, and invasion of A549 lung adenocarcinoma cells were investigated. The results showed that daphnetin inhibited the proliferation, colony formation, migration, and invasion of A549 cells through the MAPK/STAT3/NF-KB pathway, and mainly inhibited the clonal formation and migration of A549 cells through the JNK pathway. These results provide a new research direction and theoretical basis for the use of daphnetin in the inhibition of lung adenocarcinoma.

Molecule interacting with CasL 1 (MICAL1) is a crucial protein involved in cell motility, axon guidance, cytoskeletal dynamics, and gene transcription. This pan-cancer study analyzed MICAL1 across 33 cancer types using bioinformatics and experiments. Dysregulated expression, diagnostic potential, and prognostic value were assessed. Associations with tumor characteristics, immune factors, and drug sensitivity were explored. Enrichment analysis revealed MICAL1's involvement in metastasis, angiogenesis, metabolism, and immune pathways. Functional experiments demonstrated its impact on renal carcinoma cells. These findings position MICAL1 as a potential biomarker and therapeutic target in specific cancers, warranting further investigation into its role in cancer pathogenesis.

Copines are a family of calcium-dependent membrane-binding proteins. To study these proteins, anull mutant for cpnC was created in Dictyostelium, which has six copines genes (cpnA-cpnF). During development, cpnC^- cells were able to aggregate, but did not form streams. Once aggregated into mounds, they formed large ring structures. cpnC^- cells were less adherent to plastic substrates, but more adherent to other cells. These phenotypes correlated with changes in adhesion protein expression with decreased expression of SibA and increased expression of CsaA in developing cpnC^- cells. We also measured the expression of RegA, a cAMP phosphodiesterase, and found that cpnC^- cells have reduced RegA expression. The reduced RegA expression in cpnC^- cells is most likely responsible for the observed phenotypes.