ATF3 (Activating Transcription Factor 3)

Transcriptomic analyses of Egr1-deficient tumors suggested immune dysregulation, including heightened inflammation and potential markers of T cell exhaustion in the tumor microenvironment. These findings indicate that Egr1 may play a role in suppressing tumor growth through modulating immune dynamics, offering new insights into the interplay between tumor progression and immune regulation in lung adenocarcinoma.

In summary, paclitaxel induces transcriptomic and proteomic signatures of the neuronal stress response, neuroinflammation, nociception, and disturbed metabolism. These may explain, in part, the clinical phenotype of sensory loss, hypersensitivity, and neuropathic pain frequently observed in patients suffering from CIPN, but constitute pharmacologically addressable targets.

Erastin (ER), a small-molecule compound, induces ferroptosis through ROS accumulation...Our findings highlight ASNS, CHAC1, PCK2, DDIT4, and ATF3/4 as potential biomarkers for ferroptosis in CRC. Monitoring the expression of these genes may help identify patients who are responsive to ferroptosis inducers and facilitate the development of personalized treatment strategies.

This trimer stabilizes STAT3-enhancer-promoter loops (EPLs), thereby reinforcing the Tns1 transcription and facilitating CRCLM. Our findings elucidate the mechanism by which E. coli-induced NETs promote CRCLM through epigenetic modifications, offering an insight into the role of EPLs in immune regulation and tumor progression.

Genetic ablation of Trem2 or pharmacologic targeting with antisense oligonucleotides suppress paclitaxel-induced breast cancer lung metastasis in vivo. Collectively, our findings demonstrate that paclitaxel, but not nab-paclitaxel, stimulates TREM2 expression and expands TREM2+ macrophages, suggesting that TREM2 targeting could enhance paclitaxel efficacy while limiting metastasis.

ISL1 serves as both a predictive biomarker and functional dependency, as evidenced by essentiality for cell survival and loss following treatment. Prospective studies using ISL1 as a predictive biomarker for lurbinectedin are planned.

Together, our data suggest that impairment in mitochondrial dynamics of sensory neurons contributes to paclitaxel neurotoxicity and, consequently, to nociception. Therefore, preventing mitochondrial fission may be a strategy to prevent PTX-induced neurotoxicity, opening a new perspective to understanding the mechanisms involved in the development of PTX-induced neuropathy.

PTX is not required for the manifestation of motor dysfunction and neuropathic pain in MOG35-55-based EAE models. Newer EAE-nPTX models have the distinct advantage of mimicking MS disease while avoiding confounding effects of pertussis toxin.

Compared with the TCM treatment control group, the TCM treatment group showed significantly elevated levels of TC, TG, LDL-C, ALT, and AST in the serum of mice(P<0.05, P<0.01), significantly reduced levels of HDL-C(P<0.01), significantly increased levels and expressions of IL-1β, IL-6, and TNF-α mRNAs in serum and liver tissue(P<0.05, P<0.01), significantly downregulated expression of ATF3 mRNA and protein(P<0.01), and significantly upregulated expressions of TLR4 and NF-κB mRNAs and proteins(P<0.05, P<0.01). Modified Xiangsha Liujunzi Decoction may ameliorate dyslipidemia-induced liver inflammation by upregulating the expression of ApoA-I, activating ATF3, and subsequently inhibiting the TLR4/NF-κB signaling pathway.

Knockdown of ATF3 or HSPA6 eliminated the antimetastatic effects of PERP.ConclusionsPERP suppresses breast cancer metastasis by inducing ATF3, which in turn activates HSPA6 transcription. This PERP-ATF3-HSPA6 axis represents a key regulatory pathway and serves as a potential therapeutic target in metastatic breast cancer.