Shepardpape3962
The number of surgical operations for elderly patients with hepatocellular carcinoma increases as the population ages. The aim of this study was to evaluate surgical and survival outcomes in elderly patients who underwent laparoscopic or open hepatectomy for hepatocellular carcinoma.
We analyzed the data of 169 patients aged 70 or over who underwent hepatectomy for hepatocellular carcinom between January 2013 and December 2018. Sixty-four pairs were selected after propensity score matching for laparoscopic or open hepatectomy for hepatocellular carcinoma. Baseline data, surgery time, length of hospital stay, postoperative complications, pathological data, overall survival, and disease-free survival were investigated.
Operative time in the laparoscopic group was longer than in the open group. Blood loss and postoperative hospital stay were shorter in the laparoscopic group than in the open group. The rate of postoperative 30-day minor or major complications was similar between the two groups. There was no significant difference in pathological data between the two groups. There was no significant difference in overall survival and disease-free survival between the two groups.
This study suggests that laparoscopic hepatectomy for elderly patients with hepatocellular carcinoma may be safe and feasible, with better short-term outcomes and similar long-term outcomes.
This study suggests that laparoscopic hepatectomy for elderly patients with hepatocellular carcinoma may be safe and feasible, with better short-term outcomes and similar long-term outcomes.
To uncover the role of LINC01980 in aggravating the progression of hepatocellular carcinoma (HCC) via targeting caspase 9.
The expression levels of LINC01980 and caspase 9 in HCC tissues and paracancer tissues were determined by qRT-PCR. The prognostic potentials of LINC01980 and caspase 9 in HCC were assessed by Kaplan-Meier method. The regulatory effects of LINC01980 and caspase 9 on the viability, clonality and apoptosis of Huh7 and Hep3B cells were examined. Finally, the interaction between LINC01980 and caspase 9 was evaluated by performing dual-luciferase reporter gene assay and rescue experiments.
LINC01980 was upregulated in HCC tissues and cells. High level of LINC01980 indicated worse prognosis in HCC patients. Knockdown of LINC01980 could attenuate viability and clonality, but induced apoptosis in Huh7 and Hep3B cells. Caspase 9 was downregulated in HCC, and its high level predicted a better prognosis in HCC patients. Overexpression of caspase 9 achieved the same regulatory effects as LINC01980 knockdown on HCC cells. Caspase 9 was the downstream target for LINC01980, and its level was negatively regulated by LINC01980. In HCC, LINC01980 regulated HCC cell behaviors by downregulating caspase 9.
Upregulation of LINC01980 in HCC predicts a poor prognosis. LINC01980 aggravates the progression of HCC via downregulating caspase 9.
Upregulation of LINC01980 in HCC predicts a poor prognosis. LINC01980 aggravates the progression of HCC via downregulating caspase 9.
Liver cancer stem cells are associated with tumor progression, metastasis, and resistance to chemotherapy. Therefore, it is important to understand the proteins that support the tumor microenvironment. The suppression of ZEB2 results from inactivation of the Wnt/β catenin pathway. Like RBM38, it suppresses tumor outgrowth and helps increase the survival of cancer patients. However, no studies have examined the direct roles of ZEB2 and RBM38 in the tumor microenvironment.
We developed an early/advanced stage liver cancer mouse model using CD133+ cell injection that mimics liver cancer in all ways. Histology, Western blotting, and immunohistochemistry analyses were used to examine cancer progression.
Histologically, the early liver cancer showed microfoci structures; the advanced cancer showed distinct morphological changes with enlarged nucleoli and cell clumping. Immunohistochemical and Western blotting analyses of CD133 and ZEB2 proteins showed similar upregulated expression as the tumor progressed. However, RBM38 expression increased dramatically in early liver cancer but was downregulated in advanced liver cancer.
ZEB2 favors a tumor microenvironment that supports liver cancer stem cell proliferation, while RBM38 expression negatively affects the tumor microenvironment and restricts liver cancer stem cell proliferation.
ZEB2 favors a tumor microenvironment that supports liver cancer stem cell proliferation, while RBM38 expression negatively affects the tumor microenvironment and restricts liver cancer stem cell proliferation.
Liver cancer is one of the most common and highly malignant cancers of the digestive system. The main aim of the present research work was to investigate the anticancer action of rosmarinic acid - a naturally occurring plant secondary metabolite. We also investigated its effects on cell apoptosis, caspase activation, cell migration and cell invasion.
Cell viability of Hep-G2 liver cancer cells was evaluated by CCK-8 assay while apoptotic studies were carried out by fluorescence microscopy using Hoechst, acridine orange (AO)/ethidium bromide (EB) and Comet assays as well as using annexin-v/propidium iodide (PI) assay for apoptosis quantification. Western blot assay was used to study the effects of rosmarinic acid on apoptosis-related protein expressions including Bax, Bcl-2 and various caspases. In vitro wound healing assay was used to evaluate the effects on cell migration while transwell chambers assay with Matrigel was used to assess the effects of rosmarinic acid on cell invasion.
Rosmarinic acid cauc acid has a potential to inhibit in vitro cancer cell growth in Hep-G2 cells by triggering apoptosis, caspase activation and suppressing cell migration and invasion and as such this molecule could be developed as a possible anticancer agent provided further studies are carried out.
To investigate whether miR-449a can regulate the biological functions of hepatocellular carcinoma (HCC) cells by targeting special AT-rich sequence binding protein 1 (SATB1).
qRT-PCR and western blot were carried out to detect the expression of miR-449a and SATB1 in normal human hepatocyte cell line HL-7702 and in HCC cells SMMC-7721, Hep3B, HepG2, and Bel-7402. miR-449a-mimics, miR-negative control (miR-NC), specifically inhibited SATB1 RNA (si-SATB1), specifically overexpressed SATB1 RNA (sh-SATB1), and negative control RNA (Si-NC) were transfected into the Hep3B and Bel-7402 cells. MTT assay, Transwell assay and flow cytometry were conducted to detect cell proliferation, invasion, and apoptosis. Dual luciferase reporter assay was performed to determine the relationship between miR-449a and SATB1.
miR-449a was highly but SATB1 was poorly expressed in HCC cells. Selleckchem AZD0095 According to the cell experiments, the up-regulation of miR-449a expression could inhibit the proliferation and invasion of HCC cells, promote their apoptosis, and significantly reduce SATB1 expression.
