ROBO1 (Roundabout Guidance Receptor 1)

These findings provide a foundation for future clinical studies and targeted interventions to enhance recovery from PFP. Future research should focus on human sample validation to enhance clinical translation.

Additionally, treatment with recombinant Slit2 protein enhanced cell proliferation, expression of α-SMA, ECM, vimentin, N-cadherin, and migration by inducing the phosphorylation of both SMAD and non-SMAD signaling in HNFs. These findings highlight the active role of Slit2 in HTS formation, offer new insights into HTS pathology, and suggest Slit2 as a potential therapeutic target for post-burn hypertrophic scarring.

We also observed that the long-term killing ability of PD-1-KO-hROBO1-CAR-NK-92 cells was achieved by inhibiting cell senescence via knocking out PD-1. These studies proposed ROBO1 as a key target for CAR-NK therapy in NSCLC and integrated hROBO1 CAR in PD-1 locus in NK cells, resulting in synergistic tumor killing effects in NSCLC, presenting a new treatment strategy for solid tumor treatment.

To understand the development of adult glioma, we demonstrate that D2HGDH and PHLDB1 should be prioritized for functional studies in IDHmut tumors. The ROBO1 region warrants further investigation in IDHwt tumors.

The expression was significantly up-regulated in prostate cancer tissues with lymph node metastasis (P<0.01) and T3 stage.In addition, COX regression univariate analysis showed that age, preoperative PSA level, Gleason and ISUP scores, T stage, lymph node metastasis and ROBO1 protein expression status were correlated with postoperative biochemical recurrence.COX regression multivariate analysis showed that ROBO1 high expression, age, preoperative PSA value and T stagewere risk factors for the prognosis of prostate cancer (P<0.05).The results of cell experiments showed that ROBO1 promoted the proliferation, migration and invasion of prostate cancer cells.The expression of TGF-β/SMAD was decreased after ROBO1 knockdown and SLIT2/ROBO1 inhibitor (P144)treatment, respectively. The high expression of SLIT2 and ROBO1 is associated with the progression and differentiation of prostate cancer.The high expression of ROBO1 is a risk factor for biochemical recurrence of prostate cancer.At the same time, ROBO1 can inhibit the migration and invasion of prostate cancer cells by regulating the TGF-β/SMAD signaling pathway.

Overexpressed circ_ROBO1 promotes NPC development by modifying the miR-324-3p/NME1 axis.

CircROBO1 might be a promising target for treating HCC radioresistance.

ROBO1-NK cells exhibited higher efficiency in eradicating primary ovarian cancer cells and lysing ovarian tumor organoids compared with primary NK cells without ROBO1-CAR modification. These findings highlight the potential of developing ROBO1-targeted CAR-NK cells from patients' PBMCs as a personalized treatment option for ovarian cancer.

Overexpression of Cdc42 partially restores the self-renewal and erythropoiesis of HSPCs in Robo1-deficient mice. Collectively, our result implicates the essential role of ROBO1 in maintaining HSPC homeostasis and erythropoiesis via CDC42.

We identified and validated plasma membrane molecules overexpressed in HCC compared to non-tumor tissue. Because GPC3, a well-known HCC-specific marker that is expressed in 75% of HCC, was identified using our approach, we are confident that that additional molecules may also represent promising HCC-selective targets. This work could facilitate the design, engineering, and testing of novel precision oncology imaging and therapeutic agents for HCC.

Nintedanib significantly enhanced the anti-tumor effects of RIT with the 90Y-B5209B without an increase in toxicity. These findings encourage further research into the potential clinical application of combining RIT with nintedanib.