Notes

Built-in Medication regarding Chemotherapy-Induced Side-line Neuropathy.
Angiogenesis plays an essential role in the development of most solid tumors by delivering nutrients and oxygen to the tumor. Therefore, anti-angiogenic therapy, particularly anti-VEGF and anti-VEGF receptor (VEGFR) therapy, has been a popular strategy to treat cancer. However, anti-angiogenic therapy does not significantly improve patients' outcomes when used alone because the cutdown of the vessels transforms tumor cells to a hypoxia-tolerant phenotype. While combining anti-angiogenic therapy with other therapies, including chemotherapy, radiotherapy, immunotherapy, and anti-epidermal growth factor receptor (EGFR) therapy, has a promising efficacy due to the vessel normalization effect induced by anti-angiogenic agents. Here, we review the characteristics of tumor angiogenesis, the mechanisms, clinical applications, and prospects of combining anti-angiogenic therapy with other therapies in the treatment of non-small cell lung cancer.Diffuse large B-cell lymphoma (DLBCL) is the most common type of non-Hodgkin lymphoma worldwide. The molecular mechanisms underlying DLBCL have not been fully elucidated, and approximately 40% of patients who undergo standard chemoimmunotherapy still present with primary refractory disease or relapse. Non-coding RNAs (ncRNAs), a group of biomolecules functioning at the RNA level, are increasingly recognized as vital components of molecular biology. With the development of RNA-sequencing (RNA-Seq) technology, accumulating evidence shows that ncRNAs are important mediators of diverse biological processes such as cell proliferation, differentiation, and apoptosis. They are also considered promising biomarkers and better candidates than proteins and genes for the early recognition of disease onset, as they are associated with relative stability, specificity, and reproducibility. In this review, we provide the first comprehensive description of the current knowledge regarding three groups of ncRNAs-microRNAs (miRNAs), circular RNAs (circRNAs), and long non-coding RNAs (lncRNAs)-focusing on their characteristics, molecular functions, as well as diagnostic and therapeutic potential in DLBCL. This review provides an exhaustive account for researchers to explore novel biomarkers for the diagnosis and prognosis of DLBCL and therapeutic targets.
Pancreatic adenocarcinoma (PAAD) is the most lethal cancer type around the world. With the in-depth exploration of the function of long non-coding RNAs (lncRNAs), the competing endogenous RNA (ceRNA) mechanism has shown its potential to partially reveal the pathogenesis of PAAD. This study aimed to construct a lncRNA-associated ceRNA network and explore ceRNA regulatory axes with experimental and prognostic value in PAAD.

First, we applied differential expression analysis in the TCGA_PAAD dataset. Then, interaction analysis and survival analysis in multiple RNA interaction databases were conducted to construct a ceRNA network. Finally, a potential regulatory axis was validated using clinical samples and cell lines by quantitative realtime PCR (qRT-PCR).

A ceRNA network comprising 13 lncRNAs, 96 miRNAs, and 30 mRNAs was successfully constructed. Survival analysis further narrowed this network to five lncRNAs, three miRNAs, and seven mRNAs, which were significantly associated with patients' overall survival. A potential regulatory axis CASC8-miR-129-5p-TOB1 was further experimentally validated. The expression of these genes was associated with clinicopathological factors and their expression trend was consistent with ceRNA mechanism. Specifically, knockdown of lncRNA-CASC8 led to the overexpression of miR-129-5p and down-regulation of TOB1, while overexpression of CASC8 showed opposite effects.

This novel ceRNA regulatory network could provide new insight into the pathogenesis of PAAD. The new regulatory axis CASC8-miR-129-5p-TOB1 might serve as a potential therapeutic target for patients.
This novel ceRNA regulatory network could provide new insight into the pathogenesis of PAAD. The new regulatory axis CASC8-miR-129-5p-TOB1 might serve as a potential therapeutic target for patients.
(
) is an oncogenic long non-coding RNA in acute myeloid leukemia. We aimed to determine
expression in colorectal cancer (CRC) and examine the influences of
on tumor behaviors of CRC cells. Furthermore, the mechanism underlying the actions of
in CRC was unveiled in detail.

Quantitative real-time polymerase chain reaction was used to detect
expression in CRC tissues and cell lines. CRC cell proliferation, apoptosis, migration, and invasion were investigated by cell counting kit-8 assays, flow cytometry, and cell migration and invasion assays, respectively. Tumor xenograft experiments were performed to evaluate the tumor growth of CRC cells in vivo. this website The interactions among
, microRNA-484 (miR-484), and
(
) were analyzed by bioinformatics prediction, RNA immunoprecipitation and luciferase reporter assay.

was upregulated in CRC tissues and cell lines.
knockdown impaired CRC cell proliferation, migration, and invasion and promoted apoptosis in vitro. Additionally,
deficiency inhibited CRC growth in vivo. Mechanistically,
functioned as a competing endogenous RNA by directly sponging miR-484, thereby enhancing
expression. Rescue experiments further corroborated that miR-484 inhibition or
overexpression reversed the inhibitory actions of
knockdown in CRC cells.

The LINC00239/miR-484/KLF12 pathway executed critical roles in CRC oncogenicity and may provide potential targets for CRC treatments.
The LINC00239/miR-484/KLF12 pathway executed critical roles in CRC oncogenicity and may provide potential targets for CRC treatments.
Currently, plenty of studies have demonstrated that lncRNAs can act as crucial roles during the progression of various tumors, including osteosarcoma (OS), and emerging evidences indicated that lncRNAs are abundant and stable in exosomes. The objective of this study is to reveal the dysregulated lncRNAs in OS plasma exosomes and explore their functions in OS.

Microarray was performed to analyze dysregulated exosomal lncRNAs. Western blot, qRT-PCR assays, and Dual-luciferase reporter assay were used to verify the interaction among cancer susceptibility 15 (CASC15), miR-338-3p, and RAB14. Cck-8, colony formation assay, and transwell assay were performed to explore and characterize the effects of CASC15 on OS cells. Animal experiments were used to verify the effects of CASC15 in vivo.

Upregulated CASC15 was observed in OS plasma exosomes compared with control, and the same expression was observed in the OS tissues and cell lines. Further assays indicated that CASC15 knockdown could restrain the proliferation, migration, and invasion of OS cells, and inhibit the growth of OS in xenograft models.
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