Circular RNA circSP5 promotes liver metastasis of colorectal cancer via SP5-mediated BAMBI transcription.

Liver metastasis of colorectal cancer (CRC) is a major cause of cancer morbidity and mortality. Circular RNAs (circRNAs) have been widely reported to be implicated in cancer metastasis. This study aims to investigate the effect of circSP5 (has_circ_0057010) on liver metastasis of CRC.

Tumor-derived exosomal miR-19b-3p facilitates M2 macrophage polarization and exosomal LINC00273 secretion to promote lung adenocarcinoma metastasis via Hippo pathway.

Numerous reports have elucidated the important participation of exosomes in the communication between tumor cells and other cancer-related cells including tumor-associated macrophages (TAMs) in microenvironment. However, the interchange of exosomes between tumor cells and TAMs in the progression of lung adenocarcinoma (LUAD) remains largely enigmatic. Herein, we discovered that LUAD cells induced the M2 polarization of TAMs and the M2-polarized macrophages facilitated LUAD cell invasion and migration and tumor metastasis in vivo.

Corrigendum: Non-coding RNAs: Emerging Regulators of Sorafenib Resistance in Hepatocellular Carcinoma.

[This corrects the article DOI: 10.3389/fonc.2019.

Non-coding RNAs: Emerging Regulators of Sorafenib Resistance in Hepatocellular Carcinoma.

As the first oral multi-target anti-tumor drug proved for the treatment of patients with advanced liver cancer in 2007, sorafenib has changed the landscape of advanced hepatocellular carcinoma (HCC) treatment. However, drug resistance largely hinders its clinical application. Non-coding RNAs (ncRNAs), including microRNAs (miRNAs), and long non-coding (lncRNAs), have recently been demonstrated playing critical roles in a variety of cancers including HCC, while the mechanisms of ncRNAs in HCC sorafenib resistance have not been extensively characterized yet.

S1PR1 promotes proliferation and inhibits apoptosis of esophageal squamous cell carcinoma through activating STAT3 pathway.

Background: Esophageal squamous cell carcinoma (ESCC) is one of the most common cancers worldwide, which lacks effective biomarkers for prognosis. Therefore, it is urgent to explore new potential molecular markers to discriminate patients with poorer survival in ESCC.

Methods: Bioinformatics analysis, qRT-PCR, and western blot were applied to investigate S1PR1 expression.

FOXM1-Mediated LINC-ROR Regulates the Proliferation and Sensitivity to Sorafenib in Hepatocellular Carcinoma.

Hepatocellular carcinoma (HCC) is the second leading cause of cancer-associated death worldwide. Indeed, despite the benefit of sorafenib in the treatment of some patients with HCC, the majority of these patients have a poor response to or intolerance of sorafenib, resulting in further tumor progression. Exploring the mechanisms underlying sorafenib resistance is essential to the treatment of HCC.

Recent progress in the emerging role of exosome in hepatocellular carcinoma.

Exosomes are small membrane vesicles 50-150 nm in diameter released by a variety of cells, which contain miRNAs, mRNAs and proteins with the potential to regulate signalling pathways in recipient cells. Exosomes deliver nucleic acids and proteins to participate in orchestrating cell-cell communication and microenvironment modulation. In this review, we summarize recent progress in our understanding of the role of exosomes in hepatocellular carcinoma (HCC).

A Novel Aurora-A Inhibitor (MLN8237) Synergistically Enhances the Antitumor Activity of Sorafenib in Hepatocellular Carcinoma.

Currently, sorafenib-based therapy is the standard treatment for advanced hepatocellular carcinoma (HCC), and there is a strong rationale for investigating its use in combination with other agents to achieve better therapeutic effects. Aurora-A, a member of a family of mitotic serine/threonine kinases, is frequently overexpressed in human cancers and therefore represents a target for therapy. Here, we investigated a novel Aurora-A inhibitor, MLN8237, together with sorafenib in HCC cells in vitro and in vivo, and elucidated the possible molecular mechanism.

Regulation and functions of MicroRNA-149 in human cancers.

MicroRNAs are small non-coding RNAs that play critical roles in the regulatory mechanisms involving cell differentiation, proliferation, apoptosis and tumorigenesis. Recent research efforts have been conducted to apply these discoveries into clinical functions, including the early diagnosis and therapeutic outcome of patients with cancer. Previous studies have shown that microRNA-149 (miR-149) is dysregulated in various human cancers and exerts its effects on tumorigenesis and tumour progression.

Long non-coding RNA ROR promotes radioresistance in hepatocelluar carcinoma cells by acting as a ceRNA for microRNA-145 to regulate RAD18 expression.

Radiotherapy plays a limited role in the treatment of hepatocellular carcinoma (HCC) due to the development of resistance. Therefore, further investigation of underlying mechanisms involved in HCC radioresistance is warranted. Increasing evidence shows that long non-coding RNAs (linc-RNAs) are involved in the pathology of various tumors, including HCC.

PU.1/microRNA-142-3p targets ATG5/ATG16L1 to inactivate autophagy and sensitize hepatocellular carcinoma cells to sorafenib.

Sorafenib is currently the only systemic agent approved for treatment of advanced hepatocellular carcinoma (HCC). However, intrinsic and acquired resistance to sorafenib remains a great challenge with respect to improving the prognoses of patients with HCC. The cyto-protective functions of autophagy have been suggested as a potential mechanism by which chemoresistance or targeted drug resistance occurs in tumour cells.