The human cervical cancer oncogene (HCCR) has been found to be overexpressed in a variety of human cancers. However, the level of expression of HCCR and its biological function in gastric cancer are largely unknown. In this study, we evaluated HCCR expression in several gastric cancer cell lines and in one normal gastric mucosal cell line. We established a 5-FU-resistant gastric cancer cell subline, and we evaluated its HCCR expression. HCCR expression levels were high in gastric cancer lines, and expression was significantly increased in the 5-FU-resistant cancer cell subline. HCCR expression affected cell growth by regulating apoptosis in the cancer cells, and it had a positive correlation with p-STAT3 expression. Western blot and luciferase reporter assays showed that the activation of STAT3 upregulated HCCR expression in a positive feedback loop model. In vivo and in vitro studies showed that HCCR plays an important role in the apoptosis induced by 5-FU. Our data demonstrate that HCCR is probably involved in apoptosis and cancer growth and that it functions as a p-STAT3 stimulator in a positive feedback loop model. In gastric cancer cells, HCCR confers a more aggressive phenotype and resistance to 5-FU-based chemotherapy.
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http://dx.doi.org/10.1038/srep24196 | DOI Listing |
Front Oncol
September 2022
Gastroenterology Unit, Department of Medical Specialties, University of Modena and Reggio Emilia and Azienda Ospedaliero-Universitaria di Modena, Modena, Italy.
Background: Though the precise criteria for accessing LT are consistently being applied, HCC recurrence (HCC-R_LT) still affects more than 15% of the patients. We analyzed the clinical, histopathological, and biological features of patients with HCC to identify the predictive factors associated with cancer recurrence and survival after LT.
Methods: We retrospectively analyzed 441 patients with HCC who underwent LT in our center.
J Biomed Nanotechnol
March 2022
First Affiliated Hospital, Anhui University of Science & Technology, Huainan, 232001, China.
Activation of the cellular signaling pathways can induce sorafenib-resistant hepatocellular carcinoma (HCC). In this work, the PI3K/mTOR inhibitor GSK1059615 inhibited the proliferation and invasion of HCC cells. PLGA-PEG-mal diblock copolymer was used to load GSK1059615 and sorafenib, and the vector was further modified with GPC3 antibody (hGC33) to obtain hGC33-modified GSK1059615 and sorafenib-loaded nanoparticles (Ab-G/S-NP).
View Article and Find Full Text PDFAm J Transl Res
March 2022
Department of Hematology-Oncology, College of Medicine, Yeungnam University Daegu, Republic of Korea.
Objective: Human cervical cancer oncogene (HCCR)-1, previously identified in cervical cancer and its cell lines, has been reported to play an important role in tumor progression in several cancers as a suppressor of apoptosis. However, the role of in the tumorigenesis of stomach cancer has not been identified. This study examined the role of as a suppressor of apoptosis during tumorigenesis in gastric cancer, along with its possible regulatory pathway.
View Article and Find Full Text PDFGynecol Endocrinol
November 2020
Department of Gynecology Oncology, Xuzhou Cancer Hospital, Xuzhou Hospital Affiliated to Jiangsu University, Xuzhou, China.
To investigate the mechanism of small nucleolar RNA host gene 1 (SNHG1) in cervical cancer (CC). The expression of SNHG1, miR-194 and human cervical cancer oncogene (HCCR) in CC tissues and cells was detected using qRT-PCR and western blot. The interaction among the three molecules was measured using dual-luciferase reporter assay and RNA immunoprecipitation assay.
View Article and Find Full Text PDFJ Immunol
March 2020
School of Life Sciences, Brain Korea 21 Plus/Kyungpook National University Creative BioResearch Group, Kyungpook National University, Daegu 41566, Republic of Korea; and
LETM1 domain-containing protein 1 (LETMD1), also known as HCCR-1, is a mitochondrial protein and is known to regulate p53 and STAT3 activities in cancer cells. In this study, we present, for the first time (to our knowledge), data indicating that LETMD1 suppresses multiple immune responses in monocyte/macrophage lineage cells and mouse primary macrophages. Attenuation of LETMD1 expression with specific small interfering RNA and short hairpin RNA constructs enhanced LPS-induced expressions of inflammatory mediators in macrophages.
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