Chemotherapy is one of the main therapeutic strategies used for gastrointestinal tract adenocarcinomas (GTAs), but resistance to anticancer drugs is a substantial obstacle in successful chemotherapy. Accumulating evidence shows that non-coding RNAs, especially long non-coding RNAs (lncRNAs) and microRNAs (miRNAs), can affect the drug resistance of tumor cells by forming a ceRNA regulatory network with mRNAs. The efficiency of the competing endogenous RNAs (ceRNAs) network can be affected by the number and integrality of miRNA recognition elements (MREs). Dynamic factors such as RNA editing, alternative splicing, single nucleotide polymorphism (SNP), RNA-binding proteins and RNA secondary structure can influence the MRE activity, which may in turn be involved in the regulation of chemoresistance-associated ceRNA network by prospective approaches. Besides activities in a single tumor cell, the components of the tumor micoenvironment (TME) also affect the ceRNA network by regulating the expression of non-coding RNA directly or indirectly. The alternation of the ceRNA network often has an impact on the malignant phenotype of tumor including chemoresistance. In this review, we focused on how MRE-associated dynamic factors and components of TME affected the ceRNA network and speculated the potential association of ceRNA network with chemoresistance. We also summarized the ceRNA network of lncRNAs, miRNAs, and mRNAs which efficiently triggers chemoresistance in the specific types of GTAs and analyzed the role of each RNA as a "promoter" or "suppressor" of chemoresistance.

Drug resistance is one of the main challenges in cancer treatment. Long non coding RNAs (lncRNAs) play a complex and precise regulatory role in regulating drug resistance of cancer. The common ways of lncRNA regulating drug resistance of cancer involve ATP binding transporter overexpression, abnormal DNA damage response, tumor cell apoptosis, accumulation of epithelial mesenchymal transformation and cancer stem cell formation. Moreover, studies on exosomal lncRNAs regulating cancer drug resistance are developed in recent years. Further study on the role and mechanism of lncRNAs drug resistance in cancer will help clinical cancer treatment program and explore new treatment methods. This paper reviews recent advances in lncRNAs regulating drug resistance of cancer, especially the role of exosomal lncRNAs.

Heilongjiang Province located in northeast China is a multi-ethnic region with people who have lived in cold conditions for several generations. Fatty acids are important to people with cold resistance. CPT1A encodes a protein that imports long-chain fatty acids into the mitochondria for fatty-acid oxidation. FADS is an essential enzyme for the synthesis of long-chain polyunsaturated fatty acids. In the present study, we investigated the distributions of three cold resistance-related SNPs (rs80356779 G > A in CPT1A, rs7115739 T > G in FADS3 and rs174570 C > T in FADS2) from six populations that included 1093 individuals who have lived in Heilongjiang Province for at least three generations. The frequencies of rs174570 and rs7115739 were different in our six north minorities compared to the Chinese Dai in Xishuangbanna (CDX) in southern China. All the SNPs in Hezhen were significantly different from other five studied populations. In addition, the genetic distribution of rs174570 in Daur was significantly different from Manchu and Korea, and the frequency of rs7115739 in Ewenki was significantly different from the other populations. The results also showed that the frequencies of the three SNPs in the six minorities were different from those of Greenlandic Inuit and Siberian population. Our results showed the distributions of the three cold resistance-related SNPs from six populations that included 1093 individuals in northern China. Distributions of the allele frequencies for the cold resistance-related SNPs in northern China were statistically different from those in southern China. These data help to establish the DNA genome database for the six populations and fully preserve existing minority genetic information.

Cisplatin-based chemotherapy has been widely used in the treatment of lung adenocarcinoma (LUAD). However, the development of cisplatin resistance becomes a major obstacle impeding the curative effect. It remains necessary to uncover the molecular mechanism of cisplatin resistance. Based on the CCLE database, lung cancer cell lines were divided into cisplatin-resistant and cisplatin-sensitive groups. The differentially expressed miRNAs were filtered and further identified by survival prognosis analysis. After transfection with miR-375 inhibitor or mimic, cell cytotoxicity assay, flow cytometry and western blot were conducted to validate the role of miR-375. The transcription factor (TF)-miRNA network was constructed based on TransmiR. The target genes of miR-375 were predicted by Starbase and further verified by RT-qPCR and immunohistochemistry results in the Human Protein Atlas. Functional enrichment analysis was performed with GO terms and KEGG. In this study, miR-375 showed the ability to promote cisplatin sensitivity and apoptosis of LUAD. Genes correlated with miR-375 in LUAD were analyzed and ABCC8 showed the strongest positive correlation. Moreover, transcription factors that regulate miR-375 expression were predicted. MBNL1, PTPN3, PRKD1 and RPN1 were identified as the target genes of miR-375. Enrichment analysis demonstrated that miR-375-related genes associated with promoting cell proliferation and anti-apoptosis were involved in the MAPK signaling pathway. Overall, this study provides new insights into the role of miR-375 in the cisplatin sensitivity of LUAD. Our present findings may serve as a theoretical basis for new therapeutic strategies and predictive models of cisplatin resistance in LUAD.