Precision diagnosis of Hepatocellular Carcinoma

Wang, Zhenxiao; Qin, Hanjiao; Shui, Lingling; Sheng, Jiyao; Zhang, Xuewen

doi:10.1097/cm9.0000000000002641

Cited by 13 publications

(4 citation statements)

References 86 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Liver cancer refers to a malignant tumor of the liver, generally referred to as primary liver cancer. According to the pathological classification, primary liver cancer may be divided into HCC and intrahepatic cholangiocarcinoma, among other types ( 55 ). HCC is the most common type of primary liver cancer ( 47 ), and is currently a hot spot of domestic and international research.…”

Section: Relationship Between Abnormal Lipid Metabolism and Cancermentioning

confidence: 99%

Long non‑coding RNAs, lipid metabolism and cancer (Review)

Zhang,

Hou,

Cao

et al. 2023

Exp Ther Med

View full text Add to dashboard Cite

Cancer has emerged as the most common cause of death in China. The change in lipid metabolism has been confirmed to have a role in several tumor types, such as esophageal, gastric, colorectal and liver cancer. Cancer cells use lipid metabolism for energy and then rapidly proliferate, invade and migrate. The main pathway by which cancer cell lipid metabolism influences cancer progression is increased fatty acid synthesis. Long non-coding (lnc)RNAs are important ncRNAs that were indicated to have significant roles in the development of human tumors. They are considered potential tumor biomarkers. Increased lipid synthesis or uptake due to deregulation of lncRNAs contributes to rapid tumor growth. In the present review, current studies on the relationship between lncRNAs, lipid metabolism and the occurrence and development of tumors were collated and summarized, and their mechanism of action was discussed. The review is expected to provide a theoretical basis for tumor treatment and prognosis evaluation based on the effective regulation of lncRNAs and lipid metabolism.

show abstract

Section: Relationship Between Abnormal Lipid Metabolism and Cancermentioning

confidence: 99%

Long non‑coding RNAs, lipid metabolism and cancer (Review)

Zhang,

Hou,

Cao

et al. 2023

Exp Ther Med

View full text Add to dashboard Cite

show abstract

“…After treatment with shikonin (0.5, 1, 2, 5, 7.5, and 10 μM) for approximately 24 h, the cell viability was assessed by CCK-8 assay. Then, the cells were treated (6,12,24,36, and 48 h) with 50 μM Nec-1 and assayed for cell viability. The WRL68 cell line was treated with different concentrations of ICG (25,50,75,100,125, and 150 μg/mL), and the cell viability was detected by CCK-8 assay.…”

Section: Cell Viabilitymentioning

confidence: 99%

“… 3 , 4 Hepatocellular carcinoma (HCC) is the main etiologic type of primary liver carcinoma. 5 , 6 The current clinical targeted therapeutics for advanced HCC, such as sorafenib, face drug resistance after several months of treatment, which reduces the therapeutic efficacy. 7 , 8 Thus, it is urgent to explore ways to improve drug resistance and the therapeutic effect of liver cancer, which is an essential research direction for HCC treatment.…”

Section: Introductionmentioning

confidence: 99%

Sonosensitizer Nanoplatforms Augmented Sonodynamic Therapy-Sensitizing Shikonin-Induced Necroptosis Against Hepatocellular Carcinoma

Tian,

Shang,

Chen

et al. 2023

IJN

View full text Add to dashboard Cite

Background Apoptosis resistance of hepatocellular carcinoma (HCC) often leads to treatment failure. Nonetheless, overcoming the resistance of HCC to apoptosis by inducing necroptosis of tumor cells to bypass the apoptotic pathway may be a promising treatment strategy. Sonodynamic therapy (SDT) has broad prospects in disease treatment because of its noninvasive characteristic and spatiotemporal control. The combination of SDT and shikonin in the treatment of HCC is expected to be a new tumor treatment method that can overcome apoptosis resistance. Methods In this study, the antitumor effect was evaluated using normal liver cell line WRL68, HCC cell line HepG2 and HepG2 xenograft mouse models. Indocyanine green (ICG) was loaded on nanobubbles (NBs) to construct ICG-loaded nanobubbles (ICG-NBs). Combined sonosensitizer nanoplatforms with ultrasound (US) to achieve efficient SDT, the combination of SDT and shikonin in treating HCC can activate shikonin-induced necroptosis. As a result, tumor cells that produced apoptosis resistance were destroyed by necroptosis. Results The results indicated a successful preparation of ICG-NBs with a uniform particle size of 273.0 ± 118.9 nm spherical structures. ICG-NB-mediated SDT, in combination with shikonin treatment, inhibited the viability, invasion, and migration of tumor cells. SDT + shikonin treatment group caused a substantial increase in necroptotic cells. The increased degree of tumor necrosis and the upregulated expression of receptor-interacting protein 3 kinase were observed in vivo studies, which indicated that the antitumor effect was accompanied by enhanced necroptosis in the SDT + shikonin treatment group. Conclusion ICG-NB-mediated SDT combined with shikonin inhibits the growth of HCC by increasing the necroptosis of tumor cells. Therefore, this combination therapy is a promising treatment strategy against the specific cancer.

show abstract

“…For early-stage HCC, alternative treatment strategies are relatively mature, such as surgical resection or radiofrequency ablation [ 3 , 4 ]. However, the early symptoms of liver cancer are very subtle and difficult to detect in a timely manner [ 5 , 6 ]. The vast majority of patients have entered the middle and late stages once diagnosed, losing the opportunity for radical surgery [ 7 - 9 ].…”

Section: Introductionmentioning

confidence: 99%

FIGNL1 Promotes Hepatocellular Carcinoma Formation via Remodeling ECM-receptor Interaction Pathway Mediated by HMMR

Wang,

Sun,

Liu

et al. 2024

CGT

View full text Add to dashboard Cite

Background:: The development of novel biomarkers is crucial for the treatment of HCC. In this study, we investigated a new molecular therapeutic target for HCC. Fidgetin-like 1 (FIGNL1) has been reported to play a vital role in lung adenocarcinoma. However, the potential function of FIGNL1 in HCC is still unknown. Objective:: This study aims to investigate the key regulatory mechanisms of FIGNL1 in the formation of HCC. Methods:: The regulatory effect of FIGNL1 on HCC was studied by lentivirus infection. In vitro, the effects of FIGNL1 on the proliferation, migration and apoptosis of cells were investigated by CCK8, colony formation assay, transwell and flow cytometry. Meanwhile, the regulation of FIGNL1 on HCC formation in vivo was studied by subcutaneous transplanted tumors. In addition, using transcriptome sequencing technology, we further explored the specific molecular mechanism of FIGNL1 regulating the formation of HCC. Results:: Functionally, we demonstrated that FIGNL1 knockdown significantly inhibited HCC cell proliferation, migration and promoted cell apoptosis in vitro. Similarly, the knockdown of FIGNL1 meaningfully weakened hepatocarcinogenesis in nude mice. Transcriptome sequencing revealed that FIGNL1 affected the expression of genes involved in extracellular matrix-receptor (ECM-receptor) interaction pathway, such as hyaluronan mediated motility receptor (HMMR). Further validation found that overexpression of HMMR based on knockdown FIGNL1 can rescue the expression abundance of related genes involved in the ECM-receptor interaction pathway. Conclusion:: Our study revealed that FIGNL1 could modulate the ECM-receptor interaction pathway through the regulation of HMMR, thus regulating the formation of HCC.

show abstract

Precision diagnosis of Hepatocellular Carcinoma

Cited by 13 publications

References 86 publications

Long non‑coding RNAs, lipid metabolism and cancer (Review)

Long non‑coding RNAs, lipid metabolism and cancer (Review)

Sonosensitizer Nanoplatforms Augmented Sonodynamic Therapy-Sensitizing Shikonin-Induced Necroptosis Against Hepatocellular Carcinoma

FIGNL1 Promotes Hepatocellular Carcinoma Formation via Remodeling ECM-receptor Interaction Pathway Mediated by HMMR

Contact Info

Product

Resources

About