Effects of polo-like kinase (PLK1) on proliferation, migration and invasion capacities of gastric cancer cells through epithelial-mesenchymal transition (EMT) were investigated. Small-interfering ribonucleic acid (siRNA) with targeted interference in PLK1 gene was designed and transfected into gastric cancer MGC-803 cells via Lipofectamine to inhibit the expression of PLK1 gene in MGC-803 cells. The proliferation of MGC-803 cells was detected via methyl thiazolyl tetrazolium (MTT) assay. The mRNA and protein expression of PLK1 and EMT-related marker (E-cadherin) was detected via real-time polymerase chain reaction and western blot analysis, respectively. The effects of interference in PLK1 gene on migration and invasion of MGC-803 cells were studied via wound healing assay and Transwell chamber assay, respectively. Results of MTT assay showed that compared with that in control group, the cell proliferation in PLK1 siRNA group was significantly inhibited (p<0.01). Compared with those in control group, the mRNA and protein expression of PLK1 in PLK1 siRNA group was significantly decreased (p<0.01), but the mRNA and protein expression of E-cadherin was obviously upregulated (p<0.01). Results of wound healing assay and invasion assay showed that the capacity of migration and invasion of MGC-803 cells in PLK1 siRNA group was significantly inhibited compared with those in control group (p<0.01). In conclusion, PLK1 enhances the proliferation, migration and invasion of gastric cancer MGC-803 cells through affecting EMT.

The aim of the present study was to detect mutations in the coding genes of mitochondrial DNA (mtDNA) in three esophageal cancer cell lines and in tumor tissues obtained from 30 patients with esophageal cancer, to investigate the relationship between protein‑ and RNA‑coding gene mutations and esophageal cancer. mtDNA was extracted and the coding genes were sequenced and analyzed by comparing the sequencing results with the complete mitochondrial genome of Homo sapiens. The results revealed 39 mutations in the three esophageal cancer cell lines; the genes with the highest mutation frequencies included mitochondrially encoded cytochrome B (MT‑CYTB), NADH dehydrogenase 5 (MT‑ND5) and MT‑ND4 gene. A total of 216 mutations were identified in the 30 esophageal cancer tissues, including 182 protein‑coding mutations, of which MT‑CYTB and MT‑ND5 genes exhibited higher mutation frequencies. The results of the present study indicated that mutations in the coding genes of mtDNA in esophageal cancer cells may be related to the occurrence of esophageal cancer.

To investigate the therapeutic effect of conversion therapy and its correlation with vascular endothelial growth factor (VEGF) expression in unresectable rectal cancer with liver metastasis. A total of 116 cases of unresectable rectal cancer patients with liver metastasis were randomly divided into control and observation group, 58 cases in each group, all of these patients were treated by conversion therapy, patients in control were treated by FOLFOXIRI treatment program, and in observation group were treated by FOLFOXIRI program treatment and bevacizumab. Efficacy and adverse reactions were compared between the two groups, the levels of VEGF in portal vein and the expression of VEGF in cancer tissue were compared, after 5 years of follow-up, the prognosis of the two groups were observed. Objective efficiency and conversion rate of observation was significantly higher than the control group, survival rate of postoperative observation was significantly higher than that of control group (P>0.05). There was no significant difference in adverse reactions between the two groups (P>0.05). The positive rate of VEGF in portal vein blood and the expression of VEGF in the observation was significantly lower than that in the control group (P<0.05). The 5-year survival rate of VEGF high expression was significantly lower than that of VEGF low expression group (P<0.05). FOLFOXIRI combined with bevacizumab in patients with unresectable hepatic metastasis of rectal cancer can provide higher conversion rate and hepatectomy opportunities, and reduce VEGF expression in patients with unresectable rectal cancer, which is closely related to VEGF expression, therefore it is beneficial to better local control and to improve long-term survival.

e17509 Background: Anlotinib is a novel small molecule antiangiogenic drug, which can inhibit multiple tyrosine kinase receptor activity. Its antitumor activity has been proved in various cancers, including gynecological tumors. This retrospective study explored the efficacy and safety of anlotinib monotherapy or anlotinib combined chemotherapy in cervical cancer patients who have disease progressed or metastasis after chemoradiotherapy. Methods: 28 patients with cervical cancer admitted to the Second Affiliated Hospital of Zhengzhou University were enrolled. These patients who had received radiotherapy and at least one line chemotherapy had tumor progression or metastasis. 13 patients received anlotinib monotherapy (12mg/d from day 1 to day 14 in a 21-day cycle) and 15 patients received chemotherapy combined with the anlotinib. Treatment was continued until disease progression or death or intolerable adverse events. The primary endpoint was the objective response rate (ORR), and the secondary endpoints were disease control rate (DCR), progression-free survival (PFS) and safety. Results: As of Dec 31 2020, no one was lost follow up. 2 patients were still under treatment, and 26 patients were evaluable. 1 CR, 6 PR, 13 SD, 6 PD, yielding the ORR of 26.92%, and the DCR of 76.92%. The median PFS for receiving anlotinib monotherapy was 4.57 (95% CI, 3.85-5.29) months, and 8.47 (95% CI, 5.09-11.85) months for combination group. The most common adverse events (AEs)were grade 1, including hypertension (46.43%), anemia (42.85%) and fatigue (39.29%). Grade 3 AEs were hypertension(10.71%) and anemia(7.14%). No higher grade AEs occurred. Conclusions: Anlotinib is safe and effective for patients with advanced cervical cancer after chemoradiotherapy, and it is well tolerated.

The present study aimed to detect the mutation characteristics of mitochondrial DNA (mtDNA) in Eca109 of Ec9706 cells, and to investigate their association with the nuclear genome (nDNA), thus providing a basis for gene targeting therapies for esophageal squamous cell carcinoma (ESCC). In vitro-cultured Ec9706 and Eca109 cells were analyzed the changes of single-nucleotide polymorphisms (SNPs), insertions/deletions (INDELs), copy number variation, and structure variation (SV) of their genome by high-throughput sequencing. The loci with SV on chromosome 1–12 of the two ESCC cell lines were ≥5% of the mtDNA, but SV on chromosome 13–22, X and Y was ≤3%; >40% of loci exhibited gain or loss; intergenic loci with INDEL changes and SNP features accounted for the majority of mutations. The affected genes encoded proteins including nDNA-encoding intra-mitochondrial-transporting proteins, ATP energy generation-associated proteins and mitochondrial electron respiratory chain proteins, and these proteins were all nucleus-encoded mitochondrial proteins. The transcription, duplication, and translation of the abnormally expressed mtDNA in Ec9706 and Eca109 cells were closely associated with disorders of nuclear DNA products.