FCN3 inhibits the progression of hepatocellular carcinoma by suppressing SBDS-mediated blockade of the p53 pathway

Ma, Dong; Liu, Pengpeng; Wen, Ji; Gu, Yang; Yang, Zhangshuo; Lan, Jianwei; Fan, Haining; Liu, Zhisu; Guo, Deliang

doi:10.7150/ijbs.69784

Cited by 12 publications

(10 citation statements)

References 44 publications

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“…The overexpression of FCN3 has been shown to inhibit cell proliferation and induce apoptosis via the p53 signaling pathway 26 . A proposed mechanism is that FCN3 modulates the nuclear translocation of eukaryotic initiation factor 6 (EIF6) by binding to ribosome maturation factor (SBDS), which then leads to activation of the p53 pathway.…”

Section: Discussionmentioning

confidence: 99%

“…A proposed mechanism is that FCN3 modulates the nuclear translocation of eukaryotic initiation factor 6 (EIF6) by binding to ribosome maturation factor (SBDS), which then leads to activation of the p53 pathway. In addition, Y-box binding protein 1 (YBX1) has been shown to regulate the translation and transcription of FCN3 to SBDS 26 . These results indicate that the FCN3/YBX1/SBDS axis may be a novel therapeutic target for HCC.…”

Section: Discussionmentioning

confidence: 99%

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Loss of ficolin-3 expression is associated with poor prognosis in patients with hepatocellular carcinoma

Chen¹,

Yu²,

Wu³

et al. 2023

Int. J. Med. Sci.

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Background: Ficolin-3 (FCN3) is a well-known circulating pattern recognition molecule which plays a role in host immune responses to cancer via activation of the lectin complement pathway. Nevertheless, the clinical significance of FCN3 in patients with hepatocellular carcinoma (HCC) is unclear. Methods: Eighty-seven HCC patients who received hepatectomy at our hospital were included. Immunohistochemical staining was used to assess the FCN3 expression in both tumorous and non-tumorous tissues from the patients, who were classified into high and low expression groups. Differences in clinicopathological characteristics between the two groups were then analyzed. Results: Survival was significantly associated with FCN3 immunohistochemical score (p for trend = 0.048). Kaplan-Meier analysis revealed a higher overall survival rate in the patients with a high FCN3 expression than in those with a low FCN3 expression (p=0.031). A high FCN3 expression in tumor tissue was independently associated with better overall survival (p=0.042). However, multivariate analysis showed that FCN3 expression was not an independent risk factor for overall survival. Conclusion: Our findings suggest that FCN3 is significantly related to the prognosis of HCC. FCN3 may be a prognostic marker in patients with HCC.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Loss of ficolin-3 expression is associated with poor prognosis in patients with hepatocellular carcinoma

Chen¹,

Yu²,

Wu³

et al. 2023

Int. J. Med. Sci.

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“…As shown in Figure 2, the activation of p53 mainly involves biological mechanisms such as acetylation and phosphorylation, while the inactivation of p53 is closely related to its ubiquitination, ubiquitination, and partial dephosphorylation 1,137 . At the same time, various proteins are not only activated by the transcription of p53 but also participate in the regulation of p53 activation or inactivation 138 . p53 and these proteins constitute a complex feedback regulatory network, including Siva1, 139 COP1, 140 Pirh2, 140 cyclin G, 141 ΔNp73, 142 and so on, as well as the classic MDM2 143 …”

Section: Activation and Inactivation Of P53mentioning

confidence: 99%

“… 1 , 137 At the same time, various proteins are not only activated by the transcription of p53 but also participate in the regulation of p53 activation or inactivation. 138 p53 and these proteins constitute a complex feedback regulatory network, including Siva1, 139 COP1, 140 Pirh2, 140 cyclin G, 141 ΔNp73, 142 and so on, as well as the classic MDM2. 143 …”

Section: Activation and Inactivation Of P53mentioning

confidence: 99%

Targeting the p53 signaling pathway in cancers: Molecular mechanisms and clinical studies

Shen¹,

Wang²,

Mao³

et al. 2023

MedComm

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Tumor suppressor p53 can transcriptionally activate downstream genes in response to stress, and then regulate the cell cycle, DNA repair, metabolism, angiogenesis, apoptosis, and other biological responses. p53 has seven functional domains and 12 splice isoforms, and different domains and subtypes play different roles. The activation and inactivation of p53 are finely regulated and are associated with phosphorylation/acetylation modification and ubiquitination modification, respectively. Abnormal activation of p53 is closely related to the occurrence and development of cancer. While targeted therapy of the p53 signaling pathway is still in its early stages and only a few drugs or treatments have entered clinical trials, the development of new drugs and ongoing clinical trials are expected to lead to the widespread use of p53 signaling‐targeted therapy in cancer treatment in the future. TRIAP1 is a novel p53 downstream inhibitor of apoptosis. TRIAP1 is the homolog of yeast mitochondrial intermembrane protein MDM35, which can play a tumor‐promoting role by blocking the mitochondria‐dependent apoptosis pathway. This work provides a systematic overview of recent basic research and clinical progress in the p53 signaling pathway and proposes that TRIAP1 is an important therapeutic target downstream of p53 signaling.

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“…Imbalances in plasma protein expression are frequently linked to pathological processes, particularly tumorigenesis. Numerous studies have reported positive (16)(17)(18)(19)(20)(21)(22)(23) or negatively (24)(25)(26)(27)(28)(29)(30)(31)(32)(33) correlations between plasma protein levels and tumor development, indicating that plasma protein levels may be in uenced by tumors or play a role in promoting or inhibiting tumor growth.…”

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confidence: 99%

Cathepsins Influence Metastatic Liver Cancer via Plasma Proteins: a Mendelian randomization Study

Yi,

Lin,

Zhong

et al. 2024

Preprint

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Background: Cathepsins (CTSs), lysosomal cysteine proteases, have been reported to play roles in the initiation, infiltration, and dissemination of tumors in previous researches. However, the precise causal relationship between CTSs and metastatic liver cancer (MLC) remains undetermined. This study aimed to investigate the potential causal relationship between CTSs and MLC, as well as to examine the mediating effect of plasma proteins in this relationship, ultimately establishing a causal network among them. Methods: Data were obtained from genome-wide association analysis (GWAS). Inverse variance weighting (IVW), Bayesian weighting (BW), MR-Egger regression, Weighted median (WM) and MR-conmix methods were employed for Mendelian randomization (MR) Analysis. Sensitivity analysis included Cochran's Q test, Mr-Egger intercept, MR-PRESSO test and leave-one-out validation. Results: Univariable MR revealed that an increase in CTSF (cathepsin F), CTSD (cathepsin D), and CSTV (cathepsin V) was associated with a reduced risk of MLC among 11 CTSs. While reverse MR did not yield significant findings. And total of 42 plasma proteins were identified to have a causal relationship with MLC, among which 13 types were found to mediate the association between the 3 CTSs and MLC. Conclusions: Our study suggests a potential causal relationship involving 3 CTSs, 13 plasma proteins, and MLC. These results provide valuable references for disease prediction, targeted therapy and mechanistic research of MLC.

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FCN3 inhibits the progression of hepatocellular carcinoma by suppressing SBDS-mediated blockade of the p53 pathway

Cited by 12 publications

References 44 publications

Loss of ficolin-3 expression is associated with poor prognosis in patients with hepatocellular carcinoma

Loss of ficolin-3 expression is associated with poor prognosis in patients with hepatocellular carcinoma

Targeting the p53 signaling pathway in cancers: Molecular mechanisms and clinical studies

Cathepsins Influence Metastatic Liver Cancer via Plasma Proteins: a Mendelian randomization Study

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