Monitoring of Heat Shock Response and Phenotypic Changes in Hepatocellular Carcinoma After Heat Treatment

Insufficient ablation promotes the metastasis of residual non-small cell lung cancer (NSCLC) cells via upregulating carboxypeptidase A4

“…In HCC, several studies have found that insufficient ablation enhances the invasion and migration abilities of residual tumors. Some have found that sublethal thermal stimulus induced by insufficient ablation can induce EMT in residual HCC cells and breast cancer cells [15,16,18,29]. Other studies have also found that sublethal thermal stimulus lead to the differentiation of viable HCC cells into cancer stem cells [11,[30][31][32].…”

“…Heat treatment was simulated in vitro according to a previously reported procedure [15][16][17][18]. Adherent monolayers of A549 and H1975 cells were grown to 70% confluence, and 5 Â 10 5 cells were suspended in 1 ml DMEM, collected in 1.5 ml Boilproof Microtubes (MCT-150-B, Axygen, Corning, NY), and immediately exposed to heat stimulus using a digital dry bath incubator (CHB-100, KeHuai Instrument, Jiangsu, China) at temperature settings of 37 C, 42 C, 44 C, 46 C, 48 C, and 50 C for 10 min.…”

Direct treatment versus indirect: Thermo‐ablative and mild hyperthermia effects

“…In addition, “current understanding of the secondary effects of [thermo‐ablative] hyperthermia is often extrapolated from literature on low‐temperature hyperthermia” (Chu & Dupuy, 2014). Furthermore, expression and release of HSP70 seems to be greatest in subablative hyperthermia (Zaimoku et al, 2019). Although further study is needed, these results at least suggest the possibility that the immune response generated by thermo‐ablative hyperthermia is actually caused by mild hyperthermia generated as a side effect of thermo‐ablative hyperthermia.…”

An Overview of Hepatocellular Carcinoma After Insufficient Radiofrequency Ablation

“…In the transition zone, tumors suffer reversible damage and eventually survive, thus leading to rapid tumor progression in a activate state. 18 , 19 The mechanism is complicated after IRFA and may include the following aspects: 1) IRFA causes Epithelial Mesenchymal Transitions (EMT), which is an important cause of tumor metastasis; 20–36 2) IRFA leads to autophagic survival and plays a role in subsequent progression and metastasis; 37–44 3) IRFA causes a significant increase in the number of cancer stem cells; 21 , 24 , 31 , 37 , 45–47 4) IRFA triggers a hypoxic microenvironment that aids tumor cell survival and proliferation; 24 , 34 , 38 , 44 , 48–51 5) IRFA causes sustained local inflammation with predominant myeloid suppressor cells, which inhibits the function of T cells in tumors; 52 6) Heat shock response aids tumor cell survival after IRFA; 21 , 25 , 39 , 43 , 47 , 53 7) IRFA stimulates the expression of several growth factors and receptors; 24 , 36 , 42 , 46 , 48 , 49 , 54–57 8) IRFA activates non-tumor cells such as hepatic stellate cells (HSCs), tumor-associated endothelial cells, and platelets to help tumor cell survival and metastasis; 10 , 27 , 30 , 42 , 45 , 58 9) IRFA causes epigenetic changes; 26 , 31 , 32 , 34 10) IRFA enhances metabolic reprogramming of HCC. 30 , 34 The above mechanisms do not exist independently, but contribute to each other and together increase the malignancy of residual viable tumors.…”

“… 75–77 Sub-lethal heat treatment or hypoxic environments can lead to the generation of tumor stem cells. Among studies involving IRFA and HCC, CD133, 21 , 37 , 45–47 CD90, 24 CD44, 46 , 47 EpCAM, 45 , 46 Nanog 31 , 45 and OCT4 31 are reported to be induced. Zhang et al reported similar expression trends of CD133 with CD31 and VEGFA in the IRFA-liver cancer tissue, suggesting that IRFA may affect tumor angiogenesis through CSCs, 57 and similar findings have been reported by other studies.…”