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ave significantly improved OS and PFS, a reduced level of VEGF and a lower incidence rate of adverse reactions, so Endostatin+TAI+TACE is worthy of clinical popularization and application.

Gastric carcinoma is the fourth leading cause of cancer-related morbidity throughout the globe. There are limited clinical therapies for gastric cancer due to lack of effective drugs and ambiguity in molecular mechanisms. As such there is a pressing need for novel and effective anticancer drugs for gastric cancer. The main aim of the current research work was to investigate the anticancer effects of Lanostane natural product in MKN-45 human gastric cancer cells along with evaluating its effects on cell autophagy, apoptosis, and m-TOR/PI3K/AKT signalling pathway.

MTT cytotoxicity assay was used to evaluate cell viability of MKN-45 human gastric cancer cells. Apoptosis was evaluated by fluorescence microscopy using Hoechst 33258 and Annexin-V/propidium iodide (PI) assay using flow cytometry. Autophagy was evaluated by transmission electron microscopy (TEM) and western blot method. RMC-4630 Effects on m-TOR/PI3K/AKT related protein expression were evaluated by western blot method.

Lanostane molecule led to substantial and dose-dependent growth inhibitory effects onMKN-45 human gastric cancer cells. Clonogenic assay showed significant decrease in MKN-45 cell colonies. Hoechst 33258 and annexin V/PI revealed that lanostane induced dominant apoptotic effects in these cells and exhibited dose-dependence. TEM revealed that lanostane induced autophagy in MKN-45 cells by forming autophagosomes and autophagic vacuoles. Lanostane also targeted m-TOR/PI3K/AKT signalling pathway by altering the expression of some key proteins.

Lanostane displayed strong anticancer effects in MKN-45 human gastric cancer cells by triggering apoptosis and autophagy and targeting m-TOR/PI3K/AKT signalling pathway.

Lanostane displayed strong anticancer effects in MKN-45 human gastric cancer cells by triggering apoptosis and autophagy and targeting m-TOR/PI3K/AKT signalling pathway.

Paired related homoeobox 1 (PRRX1) has been identified as a new epithelial-mesenchymal transition (EMT) inducer in gastric cancer and that PRRX1 upregulation is closely correlated with gastric cancer metastasis. In addition, circulating tumor cells (CTCs) play an important role in the process of gastric cancer's distant metastasis. Our study aimed to correlate Prrx1, CTCs and the clinicopathological parameters in primary gastric cancer patients.

Expressions of PRRX1 in a sample of 95 gastric carcinoma and adjacent nontumorous tissues were detected by immunohistochemistry. Then the integrated subtraction enrichment and immunostaining fluorescence in situ hybridization (SET-imFISH) platform were applied to detect and characterize CTCs in patients with gastric cancer. Finally, their correlations with clinicopathological parameters could be analyzed.

The positive rate of PRRX1in gastric cancer was 56.84% and the rate was 36.84% in adjacent normal gastric mucosa, which was confirmed to be statistically signitoring and prognosis of gastric cancer.

Colorectal cancer is one of the deadly malignancies and is one of the top three most common cancers and the third leading cause of cancer-related deaths. The main objective of the study was to investigate the anticancer effects of norwogonin - a naturally occurring plant flavone. We also examined its effects on programmed cell death, autophagy and cell cycle phase distribution.

Cell viability of colon cancer cells was evaluated by MTT assay while apoptotic studies were carried out by fluorescence microscopy using acridine orange (AO)/ethidium bromide (EB) and Comet assays. Transmission electron microscopy (TEM) was used to study formation of autophagosomes reminiscent of autophagy. Furthermore, western blot assay was used to study the effects of norwogonin on apoptosis-related protein expressions including Bax, Bcl-2 and autophagy-related proteins. Effects on cell cycle were evaluated by flow cytometry.

The results showed that norwogonin causes substantial reduction in the viability of the human colorectal carcinoma cells in a dose-dependent manner, exhibiting an IC50 of 15.5 µM in cancer cells and IC50 of 90 µM in normal cell lines. The AO/EB staining assay showed that norwogonin suppresses the viability of cancer cells via induction of apoptotic cell death which was associated with increase in Bax and decrease in Bcl-2 levels. Comet assay results also confirmed that norwogonin induces apoptosis. Norwogonin also led to induction of autophagy along with triggering G2/M phase cell cycle arrest.

In conclusion, the current study shows that norwogonin has a potential to inhibit in vitro colorectal cancer cells growth by triggering apoptosis, autophagy and cell cycle arrest and as such could be developed as a possible anticancer agent.

In conclusion, the current study shows that norwogonin has a potential to inhibit in vitro colorectal cancer cells growth by triggering apoptosis, autophagy and cell cycle arrest and as such could be developed as a possible anticancer agent.

The present study was done to measure the serum relative expression levels of microRNA-18a, microRNA-21, and microRNA-92a in colorectal cancer patients compared to healthy volunteers to evaluate their use as diagnostic markers in colorectal cancer patients.

The relative serum quantification of each of microRNA-18a, microRNA-21, and microRNA-92a normalized to microRNA-16 was studied in 50 patients diagnosed with colorectal cancer and 50 age- and sex-matched healthy volunteers using real-time polymerase chain reaction (RT-PR).

The expression levels of microRNA-18a, microRNA-21, and microRNA-92a were found to be significantly up-regulated in serum of colorectal cancer patients compared to the healthy control group. MicroRNA-18a demonstrated an area under the receiver operating characteristics curve of 0.906; microRNA-21 yielded an AUC of 0.918, while microRNA-92a demonstrated an area under the receiver operating characteristics curve of 0.672 when discriminating colorectal cancer patients from healthy controls.