The significance of CDT1 expression in non-cancerous and cancerous liver in cases with hepatocellular carcinoma

Q: What was the main purpose of analyzing CDT1 in this HCC study?

To clarify the clinical significance and possible pathogenesis of CDT1 expression by comparing non-cancerous and cancerous liver tissues in HCC cases.

Q: With which proteins was CDT1 co-localized, and why is this important?

CDT1 co-localized with P57kip2, Fbwx7, P53, and c-Myc in the nucleus or cytoplasm of hepatocytes and cancer cells, supporting a link between CDT1 and cellular states involved in carcinogenesis.

Sep 24, 2026

Uploaded by Franzy

Investigation focuses on chromatin licensing and DNA replication factor 1 (CDT1) expression across non-cancerous and cancerous liver tissue in hepatocellular carcinoma (HCC). CDT1 mRNA is significantly higher in cancerous liver than in noncancerous liver, linking elevated levels to inflammatory cell infiltration, increased serum transaminase, reduced hepatic spare ability, and poorly differentiated cancer-cell status. Co-localization of CDT1 with P57kip2, Fbwx7, P53, and c-Myc is observed in nuclei or cytoplasm, indicating a relationship to hepatic reserve capacity and high carcinogenic state.

LanguageEnglish

CategoryHealthcare

FormatPDF

Pages15

Reading Time38 min

AccessFree to download

Study aims and background

Methods and patient cohort

Results on CDT1 expression

Localization with related proteins

Implications for preneoplastic activity and recurrence

The significance of CDT1 expression in noncancerous and cancerous liver in cases with hepatocellular carcinoma Masahiro Ogawa,1 Mitsuhiko Moriyama,1,2,* Yutaka Midorikawa,1 Hitomi Nakamura,1 Toshikatu Shibata,1 Kazumichi Kuroda,1 Hisashi Nakayama,3 Kazunori Kanemaru,4 Toshio Miki,4 Masahiko Sugitani,5 and Tadatoshi Takayama3 1Division of Gastroenterology and Hepatology, 3Department of Digestive Surgery, Department of Medicine, 4Department of Physiology, Division of Biomedical Sciences, and 5Department of Pathology, Nihon University School of Medicine, 30-1 Oyaguchi-Kamimachi, Itabashi-ku, Tokyo 173-8610, Japan 2Sashiogi Recuperation Hospital, 1348-1 Hourai, Nishi-ku, Saitama City, Saitama 331-0074, Japan (Received 29 May, 2023; Accepted 1 August, 2023; Released online in J-STAGE as advance publication 11 August, 2023) We previously reported that chromatin licensing and DNA replication factor 1 (CDT1) expression was associated with the extent of proliferation of atypical hepatocytes and the time to postoperative recurrence in cases of hepatocellular carcinoma (HCC) . This study aimed to clarify the clinical significance or pathogenesis of CDT1 expression in both non-cancerous and cancerous liver in HCC cases, including previously published data. We investigated the association between the expression of CDT1 in non-cancerous or cancerous liver tissues and histologic findings or biochemical examination results in 62 cases. We also examined the dual localization between CDT1 and FbxW7, P57kip2, P53 and c-Myc by confocal laser scanning microscopy. CDT1 mRNA expression was significantly higher in cancerous liver than in noncancerous liver (p<0.0001) . Elevated CDT1 mRNA expression indicates a significantly degree of inflammatory cell infiltration within lobules, along with elevated serum transaminase levels, and hepatic spare decline. CDT1 mRNA was highly expressed in a group of poorly differentiated cancer cells. CDT1 co-localized with P57kip2, Fbwx7, P53 and c-Myc in the nucleus or cytoplasm of hepatocytes and cancer cells. We found that CDT1 mRNA expression could represent the degree of hepatic spare ability and the high carcinogenic state. Key Words: chromatin licensing and DNA replication factor 1, hepatocellular carcinoma, proliferation of atypical hepatocytes, Ki-67, P57 kip2 The pathogenesis of HCC development remains unclear. On the other hand, we also reported that the degree of irregular regeneration (IR) of hepatocytes were important risk factor for the development of hepatocellular carcinoma (HCC) from chronic hepatitis C (CHC) or liver cirrhosis (LC) .(1,2) Further‐ more, we have reported the extent of proliferation of atypical hepatocytes (POAH), which is one of the irregular regeneration (IR) of hepatocytes populations as a strong risk factor for the development of HCC from CHC or LC.(3) In addition, we recently examined the pathological findings of non-cancerous liver sections in 356 cases with HCC and reported that the extent of POAH was a significant factor involved in the postoperative recurrence of HCC.(4) In addition, we examined the pathological findings of noncancerous liver sections in 356 cases with HCC and reported that the extent of POAH was a significant factor involved in the post‐ operative recurrence of HCC.(4) It has been reported association with chromatin licensing and DNA replication factor 1 (CDT1) expression and pathogenesis of cancer development in many cancers.(5–9) Yu et al.(8) and Karavias et al.(9) reported that higher CDT1 expression was significantly associated with reduced overall survival, which supported our results in the previous study. Cai et al.(10) CDT1 promoted the proliferation of a cancer cell line in vitro. However, these previous reports were based on cancer nodules or cancer cell lines, not on non-cancerous tissues or human non-cancerous cell lines. We consider that the identifi‐ cation of pre-neoplastic cells by focusing on non-cancerous liver of histolo

FAQs

What was the main purpose of analyzing CDT1 in this HCC study?

To clarify the clinical significance and possible pathogenesis of CDT1 expression by comparing non-cancerous and cancerous liver tissues in HCC cases.

How did CDT1 mRNA expression differ between non-cancerous and cancerous liver?

CDT1 mRNA expression was significantly higher in cancerous liver than in noncancerous liver (p<0.0001).

With which proteins was CDT1 co-localized, and why is this important?

CDT1 co-localized with P57kip2, Fbwx7, P53, and c-Myc in the nucleus or cytoplasm of hepatocytes and cancer cells, supporting a link between CDT1 and cellular states involved in carcinogenesis.

Sep 24, 2026

Uploaded by Franzy