/pdf/cd58-loss-in-tumor-cells-confers-functional-impairment-of-1oi0anjm.pdf

CD58 loss in tumor cells confers functional impairment of CAR T cells

Background Circular RNAs (circRNAs) play an important regulatory role in various cancers, including hepatocellular carcinoma (HCC). This study aimed to investigate the function of hsa_circ_0006942 (circ-ATP5H) in hepatitis B virus (HBV)-associated HCC and its underlying mechanism. Methods The levels of circ-ATP5H, miR-138-5p and tumor necrosis factor alpha-induced protein 3 (TNFAIP3) were determined using quantitative real-time polymerase chain reaction (qRT-PCR) or Western blot assay. The copies of HBV DNA were examined using qRT-PCR. The levels of hepatitis B surface antigen (HBsAg) and hepatitis B e antigen (HBeAg) were detected via enzyme-linked immunosorbent assay (ELISA). Dual-luciferase reporter assay was used to analyze the interactions among circ-ATP5H, miR-138-5p and TNFAIP3. Results Circ-ATP5H and TNFAIP3 levels were increased, while miR-138-5p level was reduced in HBV-positive HCC tissues and cells. Knockdown of circ-ATP5H hindered HBV DNA replication and decreased HBsAg and HBeAg levels in HBV-infected cells. Circ-ATP5H silencing suppressed HBV replication and expression by regulating miR-138-5p. Moreover, miR-138-5p blocked HBV replication and expression via targeting TNFAIP3. Furthermore, circ-ATP5H up-regulated TNFAIP3 via absorbing miR-138-5p. Conclusion Circ-ATP5H promoted HBV replication and expression through modulating miR-138-5p/TNFAIP3 axis, suggesting a new biomarker for HBV-related HCC treatment.

/pdf/circ-atp5h-induces-hepatitis-b-virus-replication-and-3i8lknjkqw.pdf

Circ-ATP5H Induces Hepatitis B Virus Replication and Expression by Regulating miR-138-5p/TNFAIP3 Axis.

Hepatocellular carcinoma (HCC) is a common primary malignant tumor with a high mortality rate. Increasing evidence suggests that ribosomal protein LP1 (RPLP1) is involved in the progression of different types of cancer. Thus, the present study aimed to investigate the underlying molecular mechanism of RPLP1 in HCC progression. The cellular behaviors of Hep3b cells were assessed via Cell Counting Kit-8, colony formation, wound healing and Transwell assays. Western blot analysis was performed to detect protein expression levels, while reverse transcription-quantitative PCR analysis was performed to detect mRNA expression levels. The results demonstrated that RPLP1 was highly expressed in HCC tissues and cells, and the overexpression of RPLP1 was associated with a less favorable prognosis of patients with HCC. Notably, downregulation of RPLP1 significantly suppressed the proliferation, migration and invasion of Hep3b cells. Taken together, the results of the present study suggested that RPLP1 acts as an oncogene in HCC, and thus may be used to treat patients with HCC.

/pdf/rplp1-is-highly-expressed-in-hepatocellular-carcinoma-4ovflcjq8f.pdf

RPLP1 is highly expressed in hepatocellular carcinoma tissues and promotes proliferation, invasion and migration of human hepatocellular carcinoma Hep3b cells.

The long non-coding RNA (lncRNA) HOTAIR occupies a central position in the complex domain of cancer biology, particularly concerning its intricate interplay with the Wnt/β-catenin signaling pathway. This comprehensive review explores the multifaceted interactions between HOTAIR and the Wnt/β-catenin cascade, elucidating their profound function in cancer growth, progression, and therapeutic strategies. The study commences by underscoring the pivotal role of the Wnt/β-catenin cascade in governing essential cellular activities, emphasizing its dysregulation as a linchpin in cancer initiation and advancement. It introduces HOTAIR as a crucial regulatory entity, influencing gene expression in both healthy and diseased. The core of this review plunges into the intricacies of HOTAIR's engagement with Wnt/β-catenin signaling. It unravels how HOTAIR, through epigenetic modifications and transcriptional control, exerts its influence over key pathway constituents, including β-catenin, Wnt ligands, and target genes. This influence drives unchecked cancer cell growth, invasion, and metastasis. Furthermore, the review underscores the clinical significance of the HOTAIR-Wnt/β-catenin interplay, elucidating its associations with diverse cancer subtypes, patient prognoses, and prospects as a therapy. It provides insights into ongoing research endeavors to develop HOTAIR-targeted treatments and initiatives to facilitate aberrant Wnt/β-catenin activation. Concluding on a forward-looking note, the article accentuates the broader implications of HOTAIR's involvement in cancer biology, including its contributions to therapy resistance and metastatic dissemination. It underscores the importance of delving deeper into these intricate molecular relationships to pave the way for groundbreaking cancer treatment. 

HOTAIR: A key regulator of the Wnt/β-catenin signaling cascade in cancer progression and treatment.

The emergence of immunotherapy has revolutionized the treatment landscape for various types of cancer. Nevertheless, lung cancer remains one of the leading causes of cancer-related mortality worldwide due to the development of resistance in most patients. As one of the most abundant groups of immune cells in the tumor microenvironment (TME), tumor-associated macrophages (TAMs) play crucial and complex roles in the development of lung cancer, including the regulation of immunosuppressive TME remodeling, metabolic reprogramming, neoangiogenesis, metastasis, and promotion of tumoral neurogenesis. Hence, relevant strategies for lung cancer therapy, such as inhibition of macrophage recruitment, TAM reprograming, depletion of TAMs, and engineering of TAMs for drug delivery, have been developed. Based on the satisfactory treatment effect of TAM-targeted therapy, recent studies also investigated its synergistic effect with current therapies for lung cancer, including immunotherapy, radiotherapy, chemotherapy, anti-epidermal growth factor receptor (anti-EGFR) treatment, or photodynamic therapy. Thus, in this article, we summarized the key mechanisms of TAMs contributing to lung cancer progression and elaborated on the novel therapeutic strategies against TAMs. We also discussed the therapeutic potential of TAM targeting as adjuvant therapy in the current treatment of lung cancer, particularly highlighting the TAM-centered strategies for improving the efficacy of anti-programmed cell death-1/programmed cell death-ligand 1 (anti-PD-1/PD-L1) treatment.

Targeting tumor-associated macrophage: an adjuvant strategy for lung cancer therapy

Exosomes are a new way of the communication between the tumor cell and macrophage in the micro-environment. The macrophage can be induced to different phenotypes according to the different tumors. In the present study, long-chain noncoding RNA HOTAIR (lncRNA HOTAIR) was highly expressed in LSCC and exosomes. The pathway of exosomal lncRNA HOTAIR inducing macrophage to M2 polarization in the LSCC was investigated. The carcinoma tissues and adjacent tissues were collected from 104 LSCC cases, and the positive relationship between CD163-/CD206-M2 macrophage infiltration and clinical phase, lymph node spreading and pathological phase in LSCC was observed. To examine the role of exosomal lncRNA HOTAIR, macrophages were co-cultured with LSCC-exosomes of high lncRNA HOTAIR expression or transferred with HOTAIR mimics. It was suggested that exosomal lncRNA HOTAIR can induce macrophages to M2 polarization by PI3K/p-AKT/AKT signaling pathway. Furthermore, exo-treated M2 macrophages facilitate the migration, proliferation, and EMT of LSCC. 

https://bmccancer.biomedcentral.com/counter/pdf/10.1186/s12885-022-10210-5

Exosomal lncRNA HOTAIR induce macrophages to M2 polarization via PI3K/ p-AKT /AKT pathway and promote EMT and metastasis in laryngeal squamous cell carcinoma

/pdf/molecular-heterogeneity-of-cd30-diffuse-large-b-cell-19iemych.pdf

Molecular heterogeneity of CD30+ diffuse large B-cell lymphoma with prognostic significance and therapeutic implication

Pseudogenes are barely transcribed at normal, while the anomalous transcripts of them are mostly regarded as long non-coding RNAs (lncRNAs), which play potential functions in human tumorigenicity and development. The exact effects of pseudogene-derived transcripts on hepatocellular carcinoma (HCC) are ambiguous. According to our previous research and constructed database on the HCC-related lncRNAs, we noticed that UBE2MP1 was transcriptionally activated in HCC as a pseudogene from the ubiquitin-conjugating enzyme member UBE2M. In this study, we validated the high expression of the UBE2MP1 transcript in HCC and its adverse correlation with dismal outcomes for the patients. UBE2MP1 depletion at the transcript level significantly impaired cell proliferation and apoptosis resistance in HCC cell lines. Notably, we discovered that the UBE2MP1 transcript shared a specific sequence, binding to the miR-145-5p seed region with a typical ceRNA effect. Simultaneously, we verified an axis of miR-145-5p/RGS3 in HCC cells, which promoted cell proliferation and apoptosis resistance with significance. And modulation of UE2MP1 could remarkably affect RGS3 expression and consequentially influence HCC cell growth in vitro. And combined with the rescue experiment modulating either miR-145-5p or RGS3 furtherly indicated UBE2MP1 as an upstream regulator of the axis in promoting HCC cell growth and maintenance. Thus, our findings provide new strategies for HCC prevention and individual treatment.

https://www.aging-us.com/article/204319/pdf

Pseudogene UBE2MP1 derived transcript enhances in vitro cell proliferation and apoptosis resistance of hepatocellular carcinoma cells through miR-145-5p/RGS3 axis

Pseudogene-derived transcripts, especially those barely transcribed in normal tissues, have been regarded as a kind of non-coding RNAs, and present potential functions in tumorigenicity and tumor development in human beings. However, their exact effects on hepatocellular carcinoma (HCC) remain largely unknown. On basis of our previous research and the constructed online database for the non-coding RNAs related to HCC, a series of pseudogene transcripts have been discovered, and SNRPFP1, the homologous pseudogene of SNRPF, was found to produce an anomalously high expression long non-coding RNA in HCC. In this study, we validated the expression of the SNRPFP1 transcript in both HCC tissues and cell lines. The adverse correlation between SNRPFP1 expression and patients' outcomes was observed. And depletion of SNRPF1 in HCC cells significantly suppressed cell proliferation and apoptosis resistance. Meanwhile, the motility of HCC cells was potently impaired. Interestingly, miR-126-5p, one of the tumor-suppressive genes commonly decreased in HCC, was found negatively expressed and correlated with SNRPF1, and a specific region of SNRPF1 transcript is directly binding to miR-126-5p in a molecular sponge way. The rescue experiment by knock-out miR-126-5p significantly reversed the cell growth suppression and a higher ratio of cell apoptosis induced by SNRPF1 depletion. Lastly, we concluded that SNRPF1 is a pseudogene active in HCC, and its abnormally over-expressed transcript is a strong promoter of HCC cell progress in vitro by sponging miR-126-5p. We believe that the findings in this study provide new strategies for HCC prevention and therapeutic treatment. 

/pdf/pseudogene-snrpfp1-derived-long-non-coding-rna-facilitates-2xp64jln.pdf

Pseudogene SNRPFP1 derived long non-coding RNA facilitates hepatocellular carcinoma progress in vitro by sponging tumor-suppressive miR-126-5p

Recent research revealed methionine metabolism as a key mediator of tumor initiation and immune evasion. However, the relationship between methionine metabolism and tumor microenvironment (TME) in lung adenocarcinoma (LUAD) remains unknown. Here, we comprehensively analyzed the genomic alterations, expression patterns, and prognostic values of 68 methionine-related regulators (MRGs) in LUAD. We found that most MRGs were highly prognostic based on 30 datasets including 5024 LUAD patients. Three distinct MRG modification patterns were identified, which showed significant differences in clinical outcomes and TME characteristics: The C2 subtype was characterized by higher immune score, while the C3 subtype had more malignant cells and worse survival. We developed a MethScore to measure the level of methionine metabolism in LUAD. MethScore was positively correlated with T-cell dysfunction and tumor-associated macrophages (TAMs), indicating a dysfunctional TME phenotype in the high MethScore group. In addition, two immunotherapy cohorts confirmed that patients with a lower MethScore exhibited significant clinical benefits. Our study highlights the important role of methionine metabolism in modeling the TME. Evaluating methionine modification patterns will enhance our understanding of TME characteristics and can guide more effective immunotherapy strategies.

/pdf/a-novel-methionine-metabolism-related-signature-predicts-23nv2msf.pdf

A novel methionine metabolism-related signature predicts prognosis and immunotherapy response in lung adenocarcinoma.

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