Cancer cell membrane‐derived nanoparticles block the expression of immune checkpoint proteins on cancer cells and coordinate modulatory activity on immunosuppressive macrophages

Abstract

Cancer is the most recurrent chronic disease in the world, with human hepatocellular carcinoma (HCC) being the second leading cause of death among neoplasias. The high frequency of HCC relapse and metastasis warrants the development of new diagnostic and therapeutic procedures. In advanced stages, neoplastic cells can evade immune sur-

Nanomaterials modulate tumor-associated macrophages for the treatment of digestive system tumors

“…Consequently, TAM modulation using nanomaterials provides new possibilities for HCC treatment. Nanomaterials impede TAM infiltration [ [178] , [179] , [180] ], modulate their polarization [ [181] , [182] , [183] , [184] , [185] , [186] , [187] , [188] , [189] , [190] , [191] , [192] , [193] , [194] , [195] , [196] , [197] , [198] , [199] , [200] , [201] , [202] , [203] , [204] , [205] ], and eliminate M2-type TAMs within tumor tissues [ 206 ], thereby effectively impeding HCC onset and progression ( Fig. 5 , Fig.…”

“…In Sections 3 , 2.1.2 .1.1, nanomaterials effectively treated GC and CRC by regulating the NF-kB signaling pathway in M2-type TAMs. In HCC treatment, nanomaterials have been specifically engineered to target TAMs, thereby regulating the Nf-κb signaling pathway by modulating TLR, adenosine monophosphate (AMP), IKKβ (IkappaB kinaseβ), and ROS in TAMs [ [184] , [185] , [186] , [187] , [188] , [189] , [190] , [191] , [192] , [193] , [194] , [195] , [196] , [197] , [198] , 205 ] ( Fig. 7 ).…”

“…Bacterial therapy offers novel strategies for targeting tumors and stimulating both the innate and adaptive immune systems, resulting in altered TME immunodynamics [ 247 ]. In the following sections, we discuss the inhibitory effects of nanomaterials modified with bacterial derivatives on HCC growth via TAM polarization [ 186 , 187 ] ( Fig. 8 ).…”

“…In a mouse model of HCC lymphatic metastasis, DOX@Bio-Bac facilitated TAM polarization towards the M1 phenotype and triggered apoptosis in HCC cells [ 186 ]. Edson et al used cell membrane-derived NPs loaded with si-Myc and monophosphoryl lipid A (MPLA) derived from lipopolysaccharide (LPS) to produce MNPs-MPLA-siRNA, which specifically targets HCC cells and monocytes [ 187 ]. MNP-MPLA-siRNA effectively suppresses the activity of the c -Myc oncogene and downregulates CD47 and PD-L1 expression in HCC cells [ 187 ].…”

“…Edson et al used cell membrane-derived NPs loaded with si-Myc and monophosphoryl lipid A (MPLA) derived from lipopolysaccharide (LPS) to produce MNPs-MPLA-siRNA, which specifically targets HCC cells and monocytes [ 187 ]. MNP-MPLA-siRNA effectively suppresses the activity of the c -Myc oncogene and downregulates CD47 and PD-L1 expression in HCC cells [ 187 ]. Additionally, treatment with MNP-MPLA-siRNA decreased M2-type TAMs and increased M1-type TAMs [ 187 ].…”