VIM expression

Moreover, SPA-10091-HCl effectively inhibited tumor growth in the PC3 cells-implanted xenograft mouse model without any overt toxicity. These results indicate SPA-10091-HCl as a potential candidate for further development as a chemotherapeutic agent against CRPC.

Overexpression of MICAL-L2 stimulated cell migration, proliferation, and rendered KIRC cells insensitive to sunitinib and everolimus, two traditional therapies for KIRC. Furthermore, MICAL-L2 overexpression accelerated cancer progression and resistance to therapy in KIRC cells by interacting with its downstream regulator α-actinin-4 (ACTN4) in a Rab13-dependent manner, which reduced the degradation of ACTN4, leading to increased Vimentin expression. All these findings indicate that MICAL-L2 plays a crucial role in the progression of KIRC and suggest that MICAL-L2 may serve as a potential therapeutic target for KIRC treatment.

Our findings show that PF-477736 exerts anti-vascular remodeling effect by inhibiting phenotypic transition through the Chk1/p53/CD44 pathway in VSMCs, providing novel therapeutic strategies for preventing and treating vascular remodeling.

Immunohistochemistry (IHC) revealed positive expression for CD31, CD10, and vimentin, consistent with the diagnosis of EAS. Although EAS is a rare, aggressive, and often misdiagnosed condition, IHC can help confirm its diagnosis, and in our case, the scattered calcifications observed on CT imaging might be helpful in its differential diagnosis.

The high-throughput application of this 3D angiogenesis model was tested using propranolol to inhibit sprouting of spheroids with increased toxicity response. This study reports the development of a 3D model of IH that recapitulates angiogenic features of IH for molecular analysis and drug screening.

Pathological morphology and immunohistochemical analyses deepen our understanding of the pathological features of TSC and provide a diagnostic reference for clinicians who will encounter such cases in the future.

Likewise, in BIN-67 cells, BMP-7 was able to reduce proliferation, while in SCCOHT-1 cells this occurred only upon combined treatment with TGF-β and BMP-7. We conclude that in PDAC-derived tumor cells, NED is closely linked to EMT and TGF-β signaling, which may have implications for the therapeutic use of TGF-β inhibitors in PDAC management.

Further, METTL3-mediated m6A methylation of USP21. METTL3-mediated m6A methylation of USP21 promoted HCC progression by stabilizing H2BFS through deubiquitination.

We discuss potential molecular events underlying this transformation. This case highlights the importance of recognizing this rare variant and its implications for patient management and prognosis.

HULC promotes CRC cell proliferation, migration, and EMT through its interaction with IGF2BP2, highlighting the critical role of the HULC-IGF2BP2 axis in CRC progression. These findings identify HULC as a potential molecular target for CRC treatment and offer new insights for therapeutic strategies targeting CRC patients.

There is a trend of correlation between Vimentin expression and MVD in CNSWHO grade 4 HGG patients (P=0.07). NDRG1 exerts adverse effects on the CNSWHO grading of HGG by regulating the expression of VM and MVD in HGG patients, as well as the tumor EMT process.

This study confirmed that FE exposure promotes the onset of fibrotic lesions at pleural level, as fibrous plaques or nodules and fibrosis, through a mechanism similar to other form of asbestos. These results combined with epidemiological study reported in Biancavilla residents, corroborate the need to promote health and epidemiological surveillance plans of respiratory diseases in population living in FE contaminated sites.

These results suggest that DIF-1 inhibits the TAZ/YAP signaling pathway via GSK-3 activation. Further, it has been suggested that the inhibition of EMT induced by DIF-1 is involved with the suppression of TAZ/YAP signaling pathway.

In vitro and in vivo, exosomes with high levels of miR-20b-5p were linked to the progression of NSCLC. Our data suggest that exosomes with high levels of miR-20b-5p can increase development and metastasis of NSCLC cells by downregulating TGFBR2, which would serve as a predictive and diagnostic marker for NSCLC.

Most interestingly, the triplet treatment exhibited a safer toxicological profile than the doublet (vinorelbine plus carboplatin) currently applied in the clinical practice. Altogether, these preclinical data support the possibility of repurposing pirfenidone in combination with vinorelbine or with vinorelbine plus carboplatin for NSCLC perioperative treatment, improving therapeutic efficacy while reducing toxicity.

CXCR3B may play a positive role in suppressing HCC by attenuating natural killer cell cytotoxicity against HCC.

The results showed that the knockdown of SDC1 markedly suppressed the migration and invasion abilities of keloid fibroblasts and reduced the phenotypes of EMT by inhibiting Wnt/β-catenin signaling pathway. The authors' findings suggest that SDC1 may influences keloid fibroblasts migration and invasion through targeting Wnt/β-catenin signaling pathway mediated EMT, which supports its potential value as a therapeutic target for the treatment of keloid.

The radiosensitivity was enhanced, with the radiosensitivity enhancement ratio being 1.37±0.11 vs 1.00±0.01 (P=0.037), and after radiotherapy the expression of γ-H2AX increased. Oct4 is involved in the regulation of epithelial-mesenchymal transformation of esophageal squamous cell carcinoma, which promotes the proliferation, migration, and radioresistance of esophageal squamous cell carcinoma.

Taken together, the study has confirmed that JARID2 acts as a tumor suppressor, the downregulation of which promotes OSCC progression by regulating Epithelial-to-Mesenchymal Transition (EMT). The online version contains supplementary material available at 10.1007/s13205-024-04163-8.

In vivo experiments further confirmed that the VIM-AS1‒EPHA3 axis controlled tumor growth and the tumor microenvironment in HCC. These findings suggest that the downregulation of VIM-AS1 due to hypermethylation at cg02746869 increased EPHA3 mRNA expression via a m6A-dependent mechanism to increase HCC aggressiveness.

Intratumor administration of nanaomycin K significantly inhibited tumor growth without apparent adverse events for mice. These results indicate that nanaomycin K inhibit cell growth and EMT in TGF-β-induced advanced RCC, and that nanaomycin K is a potential candidate for the treatment of RCC.

The investigation emphasized more mechanistic approach of WFA. Understanding and targeting such integrative mechanical input in the tumor microenvironment will be a better therapeutic strategy to combat metastasis.

Besides, HERC4 overexpression reversed the effects of METTL3 silencing on the proliferation and migration as well as the levels of angiogenic factors in HCC cells. This study reveals the upregulation of METTL3 and HERC4 expression in HCC and their role in HCC by enhancing the proliferation, migration, and angiogenesis potential of HCC cells.

RhoC is highly expressed in SACC, and RhoC silencing may target the downstream ROCK1/p38MAPK/TWIST1 signaling pathway, thereby inhibiting the proliferation, invasion, migration, and EMT of SACC while promoting its apoptosis. On the contrary, miR-138-5p is lowly expressed in SACC and is a potential upstream gene of RhoC, and there may be binding sites between the two genes.

Notably, these effects were inhibited by the addition of bevacizumab. In conclusion, our findings illuminated the role of telocytes in promoting tumor progression, and confirmed their crucial regulatory role in the growth of tumor cells.

Clinical and histological features resemble high-grade endometrial carcinoma, necessitating an extensive IHC panel to narrow down differentials and confirm the diagnosis. This study highlights the histological and IHC features and emphasizes that early diagnosis plays a crucial role in disease management.

miR-20a-5p inhibitor + sh-GJA1 promoted the invasion, migration, and proliferation of colon cancer cells and EMT process. Overall, miR-20a-5p could target GJA1 to down-regulate the GJA1 expression, thereby regulating the EMT response, and ultimately promoting the progression of colorectal cancer.

Overall, APE exhibits anti-tumor effects on NSCLC via induction of apoptosis, attenuation of EMT, and its mechanism involves the suppression of the PI3K/Akt pathway. Our study offers new insights for the identification of novel drug development for NSCLC.

Furthermore, in vitro studies demonstrated that reducing CTSK expression led to significant reductions in THCA cell viability; clonogenic, proliferative, motility and migratory capacities; and the expression of key EMT-related proteins, including N-cadherin, vimentin, slug, and snail. Our results suggest that the expression of CTSK, a gene associated with the EMT, may be associated with THCA onset and progression and thus may serve as a promising prognostic biomarker.

In conclusion, the FXR was first reported as a tumor promoter that enhanced the proliferation and metastasis of breast cancer cells through regulating CBP-dependent p53 K382 acetylation. It proposes that FXR may serve as a potential therapeutic target for the treatment of breast cancer.

Olaparib-resistant xenografts were treated with olaparib, ATR inhibitor (ATRi, ceralasertib), CHK1 inhibitor (CHK1i, MK-8776) or their combinations. Our collective findings indicate that ATR/CHK1 pathway inhibition restores the olaparib efficacy in resistant BRCA1/2MUT high-grade serous OC, highlighting promising approach for olaparib rechallenge of non-responsive patients. Uncovered mechanisms might improve our understanding of acquisition and overcoming resistance to olaparib in ovarian cancer.

These cases highlight the existence of multifocal pulmonary CCST and seem to support the notion that multifocality in CCST may be associated with more protracted clinical course. Awareness of the existence of multifocal pattern is important for patient management and prognosis.

Moreover, we found that VIF-mediated nuclear dysmorphia led to defects in DNA repair. Together, our results unveil a novel role of VIFs in cancer cell nuclear dysmorphia, which is associated with genome instability.

Overall, farrerol suppresss HCC by inhibiting migration, invasiveness, the EMT, and angiogenesis, implying that farrerol could be a promising antimetastasis agent for HCC.

Euphorbia helioscopia can inhibit proliferation, invasion, and migration and induces apoptosis of NSCLC cells in vitro.

Aumolertinib combined with anlotinib can effectively inhibit NSCLC cell proliferation by downregulating the PI3K-Akt pathway, suggesting a potentially new option for NSCLC treatment.

Cisplatin activates nuclear factor-κB signaling in HNSCCs to promote TNF-α autocrine and induce RIP1/RIP3/MLKL-dependent necroptosis, thus leading to inhibition of cell proliferation.

Therefore, GATA3 could be useful as a panel of immunohistochemical stains that are used in diagnostic algorithm of vimentin-negative solid eosinophilic renal tumors. However, one should not solely rely on GATA3 as vimentin-negative solid eosinophilic renal tumors can have overlapping GATA3 expression.

FMN treatment significantly reduced the release of inflammatory cytokines and inhibited the effects of the PI3K/Akt signaling pathway on the key targets IL-4 and NOS3. Our results suggest FMN therapy as a novel therapeutic strategy for treating CRF.

Loss of vimentin in preoperative biopsies serves as an independent predictor of poor prognosis and lymph node metastases. Incorporating vimentin as a clinical marker can improve risk stratification and treatment decisions.

As p-HSP27 plays different roles in different stages of nasopharyngeal carcinoma metastasis, it can increase the migration ability of CNE2 cells and reduce its invasion ability. p-HSP27 may induce EMT changes in CNE2 by down-regulating E-cadherin, thus promoting CNE2 migration, and may inhibit CNE2 invasion by down-regulating MMPs expression.

Altogether, these results demonstrated that TiY has a strong potential for visualizing CRC by fluorescence imaging in various preclinical models, which can be further translated for clinical use such as fluorescence-guided surgery. Furthermore, our data indicate that TiY is preferentially uptaken by cells with EMT induction and progression, and overexpressing vimentin and Zeb1 in patients with CRC.