Cancer has been a major public health problem that has threatened human life worldwide throughout history. The main causes that contribute to the poor prognosis of cancer are metastasis and recurrence. Cancer stem cells are a group of tumor cells that possess self-renewal and differentiation ability, which is a vital cause of cancer metastasis and recurrence. Long non-coding RNAs refer to a class of RNAs that are longer than 200 nt and have no potential to code proteins, some of which can be specifically expressed in different tissues and different tumors. Long non-coding RNAs have great biological significance in the occurrence and progression of cancers. However, how long non-coding RNAs interact with cancer stem cells and then affect cancer metastasis and recurrence is not yet clear. Therefore, this review aims to summarize recent studies that focus on how long non-coding RNAs impact tumor occurrence and progression by affecting cancer stem cell self-renewal and differentiation in liver cancer, prostate cancer, breast cancer, and glioma.

Background: Lung cancer is the leading cause of cancer-related mortality globally. Discovering effective biomarkers for early diagnosis and prognosis is important to reduce the mortality rate and ensure efficient therapy for lung cancer patients. C-type lectin domain family 3 member B (CLEC3B) has been reported in various cancers, but its correlation with lung cancer remains elusive. Methods: The GEO, TCGA and Oncomine databases were analyzed to examine the expression of CLEC3B in lung cancer. The CLEC3B mRNA levels in 15 patient tissue samples were detected by real-time PCR and the CLEC3B protein levels in 34 patient tissue samples were detected by immunohistochemistry. A Chi-square test was performed to analyze the correlation of CLEC3B expression and clinicopathological factors. The diagnostic value of CLEC3B was revealed by receiver operating characteristic (ROC) curves. Univariate and multivariate Cox proportional hazards regression models and Kaplan–Meier plots were used to evaluate the prognostic value of CLEC3B in lung cancer. The TIMER database was used to evaluate the correlation of CLEC3B and immune infiltration. Gene set enrichment analysis revealed tumor‐associated biological processes related to CLEC3B. Results: CLEC3B is significantly downregulated in lung cancer patients compared with nontumor controls according to database analysis and patient tissue sample detection (p < 0.001). Specifically, CLEC3B is significantly downregulated in stage IA lung cancer patients (p < 0.001) and has a high diagnostic accuracy (area under the receiver operating characteristic curve > 0.9). Moreover, low expression of CLEC3B is related to poor progression-free survival (HR = 0.60, 95% CI 0.49–0.74, p = 8.3e−07) and overall survival (HR = 0.66, 95% CI 0.58–0.75, p = 2.1e−10), indicating it as a risk factor for lung cancer. Multivariate analysis value showed that low expression of CLEC3B may be an independent risk factor for disease‐free survival in lung cancer patients (HR = 0.655, 95% CI 0.430–0.996, Cox p = 0.048). In addition, we also investigated the potential role of CLEC3B in tumor-immune interactions and found that CLEC3B might be associated with the immune infiltration and immune activation of lung cancer, especially in squamous cell carcinoma. Conclusions: Our findings indicate that CLEC3B expression is downregulated in lung cancer and reveal the diagnostic and prognostic potential of CLEC3B in lung cancer and its potential as an immune-related therapeutic target in lung cancer.

Background: Hepatocellular carcinoma (HCC) remains a leading cause of cancer-related mortality globally, with limited therapeutic options available for advanced stages. Elucidating the molecular drivers of hepatocarcinogenesis holds promise for the development of targeted therapeutic strategies. Nuclear receptor-binding SET domain-containing protein 2 (NSD2), a histone lysine methyltransferase, is now recognized as a critical modulator of tumor progression. The aim of this study was to investigate the role of NSD2 in HCC. Methods: Messenger ribonucleic acid (mRNA) and protein levels were determined in 20 HCC patients, publicly available databases and HCC cell lines. The in vitro and in vivo phenotypic alterations upon NSD2 knockdown, such as cell proliferation, apoptosis, migration, invasion and xenograft tumor burden in male BALB/c nude mice, were assessed. The potential effects of NSD2 on nuclear factor kappa B (NF-κB) and matrix metalloproteinases (MMPs) were also analysed. Results: The findings revealed that NSD2 expression was markedly elevated in both HCC patients’ samples and cell lines. Elevated NSD2 expression was closely linked to poor prognosis in HCC patients. Furthermore, our experimental findings highlighted the critical role of NSD2 in enhancing the proliferation, migration, and invasion of HCC cells, while simultaneously inhibiting apoptosis both in vitro and in vivo. Notably, our research indicated NF-κB and MMPs as key mediators in these critical processes. Conclusions: In summary, NSD2 acts as a tumorigenic factor in the progression of HCC by activating the NF-κB and MMPs signalling pathways.

Background: Listeria monocytogenes (LM) is a facultative intracellular pathogen that causes food-borne infections in humans and animals. To invade and multiply within host cells, LM utilizes various strategies to precisely modulate its gene expression and to adapt to the in vivo environment. Objectives: To investigate the regulatory roles of Rli82 sRNA in the motility and pathogenicity of LM EGD-e. Methods: The Rli82 gene knock-out mutant strain, LM-ΔRli82, and the complementation strain, LM-ΔRli82/Rli82, were constructed using homologous recombination technology, and their motility and virulence, respectively, were determined. Moreover, the potential target mRNA regulated by Rli82 was predicted using TargetRNA2 software, and then the interaction between the target mRNA and Rli82 was verified by the two-plasmid reporter system. Results: The results showed that the motility of LM-ΔRli82 was significantly increased at 25°C, facilitated by the production of more flagella than LM EGD-e and LM-ΔRli82/Rli82. Furthermore, LD50 in LM-ΔRli82-infected mice was significantly increased as compared to LM EGD-e and LM-ΔRli82/Rli82, suggesting that the virulence of LM was weakened when the Rli82 gene was deleted. In addition, the mRNA level of flaA was not significantly elevated, but flaA protein was significantly higher in LM-ΔRli82 than in LM EGD-e and LM-ΔRli82/Rli82, suggesting that Rli82 might modulate the translation of flaA mRNA at the post-transcriptional level. Conclusions: Taken together, our findings for the first time revealed that Rli82 sRNA might be involved in the modulation of the expression of flaA protein, thereby influencing the mobility and pathogenicity of LM.