KLF4 (Kruppel-like factor 4)

Pharmacologic interventions using rapamycin and Jagged-1 further validated that Gln modulates the mTOR/Notch1 signaling cascade, leading to increased MUC2 expression and improved mucosal integrity. Collectively, these results demonstrate that Gln confers robust protection against RIII by regulating the mTOR/Notch1 axis, alleviating Notch1 overactivation, and promoting GC differentiation. These findings provide valuable mechanistic insight and experimental support for Gln as a potential therapeutic agent to prevent or mitigate radiation-induced intestinal injury.

This study indicates that XFC may upregulate the expression of lncRNA MEG3 and KLF4 by modulating METTL14-mediated m6A modification of lncRNA MEG3. Through this mechanism, XFC may regulate inflammatory responses and coagulation disorders, thereby improving SPP and exerting therapeutic effects on hyperinflammation-associated hypercoagulability in patients with OA.

Our findings establish KCTD15 as a pivotal regulator of TNBC stemness through modulation of the KLF4/β-catenin signaling axis. These results provide a robust preclinical rationale for developing therapeutic strategies targeting this molecular axis in TNBC management.

In CSC-enriched cells, SATB2 inhibition was associated with increased sensitivity to cisplatin and pemetrexed, concomitant with reduced OCT4 and SOX2 expression. Collectively, these findings support SATB2 as a candidate therapeutic target in MPM and suggest that SATB2 suppression may enhance chemotherapy response when combined with standard agents.

Targeting the CD200-mediated dormant niche in combination with chemotherapy and immune check point blockade (ICB) significantly eradicated the dormant tumor cells. These insights provide mechanistic understanding of tumor dormancy and treatment options for ICB relapse.

Preclinical studies demonstrate CSF-1R inhibitors (e.g., pexidartinib) disrupt LSC-TAM crosstalk, while CAR-M therapy synergizes with phagocytosis-promoting agents. Despite challenges, macrophage-targeted therapies offer transformative potential by remodeling the TME, overcoming resistance, and augmenting immunotherapy. This review outlines mechanistic insights and translational strategies to harness macrophage plasticity for leukemia treatment.

However, the expression levels of Oct3/4 and Nanog were significantly lower in both iTS-P OSKM2 and YAP9 cells than in the ES cells. These results conclude that no substantial difference is present in the characteristics between iTS-P cells induced by OSKM or YAP, and that their higher differentiation efficiency than the ES cells indicates promising potential for clinical applications.

PLCXD3 functions as a tumor suppressor in gastric cancer by inhibiting cell migration, invasion, and stemness through modulation of the Wnt/β-catenin pathway. Its downregulation may serve as a novel early diagnostic biomarker and a promising therapeutic target in gastric cancer management.

In TNBC cells, both normal- and adjacent-CM partially shifted MDA-MB-231 morphology toward a more epithelial-like state, decreasing caveolin-1 levels, while adjacent-CM increased MMP9 expression. Overall, these results reveal that adipose tissue-derived soluble factors exert significant and subtype-dependent effects on BC tumorigenicity.

The current study revealed a novel SPRED2/p53/miR-506-3p/KLF4 axis through which SPRED2 contributes to the suppression of HCC cell stemness and provides a potential new target to prevent HCC progression.

While not definitive, this evidence may potentially support the transcriptomic and splicing findings. SRPK1 inhibition may remodel the cervical cancer transcriptome in an HPV-linked manner, with SiHa cells exhibiting changes consistent with suppression of oncogenic signaling, whereas C33A cells adapt through translational and metabolic reprogramming.

KLF4 serves as a hub gate orchestrating cell crosstalk within the TME. Understanding its context-dependent functions may facilitate the development of KLF4-targeted therapies for precision oncology.