Suppression of pseudogene MT2P1 transcription induced by E2F7 inhibits hepatocellular carcinoma cell proliferation and facilitates apoptosis via preserving its parental gene.

The majority of the pseudogenes are inert in normal transcription. Their transcripts are mostly attributed to non-coding RNAs that play various functions in human tumorigenicity and progression. Distinctively, pseudogene MT2P1 is universally transcribed in hepatocytes and presents a significant decrease in hepatocellular carcinoma (HCC).

Ascending E2F7a/b ratio facilitates KLF13 transcription in hepatocellular carcinoma and correlates with the abundance of binuclear hepatocytes (ABH) modulation for short-term recurrence.

Short-term recurrence after surgery severely threatens patients' lives and leads to dismal outcomes in hepatocellular carcinoma (HCC). Our previous research proposed the abundance of binuclear hepatocytes (ABH) as an independent indicator related to the cytokinesis regulator Anillin and significantly associated with HCC recurrence. The exact mechanism of ABH modulation has not been clearly illustrated.

Paracancerous binuclear hepatocytes assessed by computer program is a novel biomarker for short term recurrence of hepatocellular carcinoma after surgery.

Hepatocellular carcinoma (HCC) is notorious for its high likelihood of recurrence even after radical surgery, which calls for effective adjuvant therapy based on more precise patient selection. The decline of the abundance of binuclear hepatocytes (ABH) in paracancerous liver tissues has been reported to indicate pathological changes in liver cells, leading to short-term recurrence within 2 years. In this research, we analyzed 34 HCC patients and 22 patients underwent liver surgery for non-HCC diseases.

Alternative splicing-related long noncoding RNA ANRIL facilitates hepatocellular carcinoma by targeting the miR-199a-5p/SRSF1 axis and impacting Anillin.

Hepatocellular carcinoma (HCC) is characterized by aberrant alternative splicing (AS), which plays an important part in the pathological process of this disease. However, available reports about genes and mechanisms involved in AS process are limited. Our previous research has identified ANRIL as a long noncoding RNA related to the AS process of HCC.