CSK overexpression

All the results showed that SEV could inhibit CRC progression via circSKA3 by increasing β-catenin ubiquitination degradation.

Mechanistically, PCSK9 could promote EMT by secreting CCL25. In conclusion, patients with ESCC may benefit from a novel therapeutic strategy based on these findings.

CircPCSK5 is highly expressed in GC and promotes the proliferation, invasion and EMT of GC cells, suggesting its potential as a prognostic biomarker and therapeutic target for GC.

Our data revealed an interfering effect of PCSK9, in cooperation with Aβ, on brain cholesterol metabolism leading to neuronal cholesterol reduction, a potentially deleterious effect. PCSK9 also exerted a neurotoxic effect, and thus represents a potential pharmacological target in AD.

PCSK9 played an important role in the progression and metastasis of colon cancer by regulation of tumor cell EMT and PI3K/AKT signaling and in the phenotypic polarization of macrophages by mediating MIF and lactate levels. Targeting PCSK9 expression or activity could be used to effectively control colon cancer.

PCSK9 overexpression predicts poor survival of APC/KRAS-mutant CRC patients. Together, cholesterol homeostasis regulator PCSK9 promotes APC/KRAS-mutant CRC via GGPP-KRAS/MEK/ERK axis and is a therapeutic target.

"Rescue" experiments revealed that miR-520 h down-modulation or CDK6 overexpression remarkably counteracted the inhibitory effect of circSKA3 knockdown on Daoy cells. circSKA3 facilitates medulloblastoma progression through miR-520 h/CDK6.

This work demonstrated that PCSK9 suppressed M2-like TAM polarization by regulating the secretion of OX40L from hepatocellular carcinoma cells. This study suggests that PCSK9 may be a potential target for HCC treatment.

PCSK9 might act as an oncogene or have an oncogenic role in the development and progression of colorectal cancer in vivo via activation of JAK2/STAT3/SOCS3 signaling.

Our study revealed Pcsk9 as a promising target for cancer immunotherapy. Pcsk9 deficiency could significantly recruit intratumoral immune infiltration, suppress tumor growth, improve tumor-free survival, and synergize with immune checkpoint inhibitors, by promoting the surface expression of MHC I molecules. Considering the availability of clinically approved anti-Pcsk9 antibodies, we believe that combining Pcsk9 inhibition with immune checkpoint blockade may offer new options for some cancer patients in the future.