Kallikrein-related peptidase 12 (KLK12) is overexpressed in cancer tissues including gastric, breast and prostate cancer. However, the role of KLK12 in colorectal cancer is not fully understood. In the present study, the level of KLK12 was determined by performing reverse transcription-polymerase chain reaction (RT-qPcR) in colorectal cancer tissues and cell lines. Lipofectamine ® 2000 was used to transfect HT-29 cells to overexpress and knockdown KLK12. cell viability, migration, invasion and apoptosis were detected by MTT, wound healing, Transwell and flow cytometry assays, respectively. The mRNA and protein expression levels of EMT-associated proteins, apoptosis-associated proteins, phosphorylated adenosine monophosphate-activated protein kinase (p-AMPK) and phosphorylated mammalian target of rapamycin (p-mTOR) were determined by RT-qPcR and western blot analysis. It was identified that the KLK12 mRNA levels were increased significantly in colorectal cancer tissues and cell lines. KLK12 small interfering RNA inhibited cell viability, migration and invasion. Furthermore, epithelial-mesenchymal transition (EMT)-associated proteins were altered by siKLK12. cell apoptosis was induced by KLK12 downregulation, which was demonstrated by the changes in apoptosis-associated proteins; however, KLK12 overexpression produced the opposite effect. SiKLK12 enhanced the expression of p-AMPK and suppressed the expression of p-mTOR, while KLK12 overexpression had the opposite effect. Promotion of KLK12 overexpression-induced cell viability was reversed by 5-aminoimidazole-4-carboxamide ribonucleotide, an activator of the AMPK signaling pathway, and rapamycin, a specific inhibitor of the mTOR signaling pathway. Taken together, the results of the present study indicated that KLK12 was overexpressed in colorectal cancer and may regulate cell behavior, potentially via the AMPK and mTOR pathways.

Background Colorectal cancer (CRC) has high mortality, and 5-fluorouracil (5-FU) is a common clinical chemotherapeutic drug. The current study aimed to investigate the role of FAT4 in chemosensitivity of CRC cells treated by 5-FU. Methods The immunohistochemistry and qRT-PCR was conducted to measure the FAT4 expression in CRC and adjacent tissues. The FAT4 expression was determined by qRT-PCR and Western blot, comparison of FAT expression between normal and several CRC cell lines was then made, so as to identify cell lines with the highest (LS174T) and the lowest (SW-620) expressions of FAT4 . The effects of 5-FU stimulation at various doses on cell viability were determined by CCK-8, and the level of FAT4 was also measured. After FAT4 knockdown in LS174T or FAT4 overexpression in SW-620 with or without pretreatment of 5-FU (30 µg/mL), cell growth, colony formation, cell migration and invasion, angiogenesis were determined by flow cytometry, wound-healing, transwell assay and tube formation assay, respectively. The expression levels of epithelial-mesenchymal transition (EMT) markers were detected by qRT-PCR and Western blot. Results FAT4 was down-regulated in CRC tissues and cells, cell viability of CRC cells was decreased. The level of FAT4 was increased with the increase of 5-FU concentrations. Moreover, 5-FU stimulation increased FAT4 expression, and reduced cell proliferation, migration, invasion, angiogenesis and cell EMT process, furthermore, such effects of 5-FU stimulation could be enhanced by FAT4 overexpression but reversed by FAT4 knockdown. Conclusions Upregulation of FAT4 could increase the sensitivity of CRC cells to 5-FU.

Objective. To evaluate the effectiveness and safety of acupuncture moxibustion therapy (AMT) for the breast cancer-related lymphedema (BCRL). Methods. Four English databases (MEDLINE, PubMed, Embase, and Cochrane CENTRAL) and four Chinese databases were searched from their inception to Feb 1, 2020. Eligible randomized controlled trials (RCTs) investigating AMT against any type of controlled intervention in patients for BCRL and assessing clinically relevant outcomes (total effective rate, circumference difference, and Karnofsky performance score) were included. The methodological quality of all selected trials was estimated in accordance with the guidelines published by the Cochrane Collaboration. Review Manager 5.3 was used to conduct analyses. Results. Twelve eligible RCTs are confirmed. Most of the trials selected are regarded as low methodological quality. Compared with Western medicine, physiotherapy, and functional training, traditional AMT has significantly higher treatment effect (RR 1.03 (95% CI: 1.22, 1.45); p<0.00001). In comparison with physiotherapy, AMT is better in reducing edema symptoms (MD = −0.77; 95% CI (−1.13–0.41); p<0.00001). Moreover, pooled results demonstrate that AMT results in better outcomes than functional training and Western medicine in improving Karnofsky performance score of BCRL patients (SMD = 0.69; 95% CI (0.38–1.00); p<0.00001). Conclusion. This systematic review and meta-analysis provides evidence that AMT is serviceable and safe in treating BCRL. With the limited number of available studies and methodology drawbacks, further high-quality RCTs with reasonable designs are still warranted.

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Anaplastic lymphoma kinase (ALK) rearrangements account for approximately 5–6% of non–small-cell lung cancer (NSCLC) patients. In this study, a case of lung adenocarcinoma harboring a novel MRPS9-ALK fusion is reported. The patient responded well to the first and second generation of ALK-tyrosine kinase inhibitors (ALK-TKIs) (crizotinib then alectinib), as her imaging findings and clinical symptoms significantly improved. At last follow-up, over 21 months of overall survival (OS) has been achieved since ALK-TKI treatment. The progression-free survival (PFS) is already ten months since alectinib. The adverse effects were manageable. The case presented here provides first clinical evidence of the efficacy of ALK-TKIs in NSCLC patients with MRPS9-ALK fusion.