[Retracted] Ruscogenin induces ferroptosis in pancreatic cancer cells.

Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that certain of the western blot data shown in Fig. 4 on p. 521 were strikingly similar to data that had already appeared in a pair of figures in a previously published article written by different authors at different research institutes in the journal .

SPIN1 accelerates tumorigenesis and confers radioresistance in non-small cell lung cancer by orchestrating the FOXO3a/FOXM1 axis.

Despite the importance of radiation therapy as a nonsurgical treatment for non-small cell lung cancer (NSCLC), radiation resistance has always been a concern because of poor patient response and outcomes. Therefore, it is crucial to identify novel targets to increase the effectiveness of radiotherapy and investigate the mechanisms underlying radioresistance. Previously, we demonstrated that Spindlin 1 (SPIN1) was related to tumour initiation and progression.

Tripartite motif 31 drives gastric cancer cell proliferation and invasion through activating the Wnt/β-catenin pathway by regulating Axin1 protein stability.

Mounting evidence has proposed the importance of the Wnt/β-catenin pathway and tripartite motif 31 (TRIM31) in certain malignancies. Our research aimed to clarify the correlation between aberrant TRIM31 expression and the Wnt/β-catenin pathway during gastric cancer (GC) oncogenesis and development. TRIM31 was drastically elevated in GC tissues and was closely associated with aggressive clinical outcomes and poor prognosis.

Positive efficacy of MH-301 as a postoperative adjunct to endoscopic sclerotherapy for internal hemorrhoids: a randomized, double-blind, placebo-controlled trial.

: Endoscopic sclerotherapy is a widely used minimally invasive procedure for internal hemorrhoids, yet postoperative symptoms remain a concern. The purpose of this study is to investigate the postoperative adjuvant efficacy of . : In this study, patients (≥18 years) with internal hemorrhoids that conformed to Goligher's classification of grade I-III received administration of MH-301 for 4 weeks following endoscopic sclerotherapy.

WWP2 drives the progression of gastric cancer by facilitating the ubiquitination and degradation of LATS1 protein.

Background: Large tumor suppressor kinase 1 (LATS1), one of the predominant components of the Hippo pathway, has been characterized as a key player controlling the proliferation and invasion of cancer cells, including gastric cancer (GC) cells. However, the mechanism by which the functional stability of LATS1 is modulated has yet to be elucidated.

Methods: Online prediction tools, immunohistochemistry and western blotting assays were used to explore the expression of WW domain-containing E3 ubiquitin ligase 2 (WWP2) in GC cells and tissues.

Low-density lipoprotein receptor-related protein 8 facilitates the proliferation and invasion of non-small cell lung cancer cells by regulating the Wnt/β-catenin signaling pathway.

Low-density lipoprotein receptor-related protein 8 (LRP8) is involved in the development of multiple tumors, including lung cancer. However, the exact mechanism by which LRP8 exerts its oncogenic role in non-small cell lung cancer (NSCLC) remains elusive. Hence, in this study, we aimed to unravel the expression and role of LRP8 in the progression of NSCLC.

The E3 Ubiquitin Ligase TRIM11 Facilitates Gastric Cancer Progression by Activating the Wnt/-Catenin Pathway via Destabilizing Axin1 Protein.

Background: Aberrant expression of tripartite motif 11 (TRIM11) and the Wnt/-catenin pathway are essential for facilitating tumorigenesis and progression in multiple types of cancer.

Aim: To investigate the molecular changes linking the dysregulation of TRIM11 and Wnt/-catenin pathway activation in gastric cancer (GC) progression.

Methods: The expression levels of TRIM11 were detected in GC tissues and cells by immunohistochemistry and western blotting.

The microRNA-381(miR-381)/Spindlin1(SPIN1) axis contributes to cell proliferation and invasion of colorectal cancer cells by regulating the Wnt/β-catenin pathway.

Our study aimed to investigate the clinical significance and biological functions of Spindlin1 (SPIN1) in colorectal cancer (CRC) tumorigenesis and progression, as well as the mechanism underlying its upregulation. The expression of SPIN1 was detected by immunohistochemistry and western blotting assays. Bioinformatics prediction and dual-luciferase reporter assays were used to determine whether microRNA-381 (miR-381) could target SPIN1.

Cullin-4B promotes cell proliferation and invasion through inactivation of p53 signaling pathway in colorectal cancer.

Cullin 4B (CUL4B) is a member of the Cullin RING E3 ligase family, which is found to be overexpressed in multiple cancers, thus facilitating tumorigenesis and progression. However, the correlation between CUL4B and p53 in colorectal cancer cells (CRC) remains to be further elucidated. In this study, we newly identified that CUL4B functions as a negative regulator of p53, thereby facilitating CRC tumorigenesis and progression.

An Assessment of Combination of the Camrelizumab With Chemotherapy in Metastatic Biliary Tract Cancers.

Background: Monoclonal antibodies that target the PD-1 receptor are emerging as promising therapeutic candidates for the treatment of biliary tract cancers (BTCs). The purpose of the current study was to assess the combination of the camrelizumab with chemotherapy as a first-line treatment for metastatic BTCs.

Methods: We conducted a prospective single-arm pilot study of PD-1 antibody (camrelizumab 3 mg/kg d1, Q2 W or Q3 W) combined with different chemotherapy regimens as first-line treatment for BTCs.

Coiled-Coil Domain-Containing 68 Downregulation Promotes Colorectal Cancer Cell Growth by Inhibiting ITCH-Mediated CDK4 Degradation.

Coiled-coil domain-containing 68 (CCDC68) plays different roles in cancer and is predicted as a tumor suppressor in human colorectal cancer (CRC). However, the specific role of CCDC68 in CRC and the underlying mechanisms remain unknown. Here, we showed that CCDC68 expression was lower in CRC than that in corresponding normal tissues, and CCDC68 level was positively correlated with disease-free survival.

Corrigendum: NUSAP1 Promotes Gastric Cancer Tumorigenesis and Progression by Stabilizing the YAP1 Protein.

[This corrects the article DOI: 10.3389/fonc.2020.

NUSAP1 Promotes Gastric Cancer Tumorigenesis and Progression by Stabilizing the YAP1 Protein.

The Yes-associated protein (YAP1) is a main effector of the canonical Hippo pathway, which contributes greatly to tumor initiation, progression, and metastasis in multiple cancers, including gastric cancer (GC). Due to limited knowledge of YAP1 upregulation in cancer, it is a great challenge of therapeutic targets toward the Hippo-YAP1 pathway. Here, we identify nucleolar spindle-associated protein 1 (NUSAP1) as a novel binding partner of YAP1.

Ruscogenin induces ferroptosis in pancreatic cancer cells.

Pancreatic cancer is characterized by aggressive and highly metastatic phenotypes. This disease exhibits a poor patient prognosis and is considered a challenge due to the limited treatment options encountered in clinical practice. Previous studies have shown that ruscogenin, a saponin found in the root of Ophiopogon japonicus, exerts a wide range of biological functions including anticancer activity.

UCHL3 promotes pancreatic cancer progression and chemo-resistance through FOXM1 stabilization.

The dysregulation of deubiquitinating enzymes has been reported to be important in the development of many human cancers, including pancreatic cancer. However, the precise role and potential mechanism of action of the deubiquitinating enzyme UCHL3 in pancreatic cancer progression and chemo-resistance, are poorly elucidated. In the current study, the consequences of UCHL3 knockdown in pancreatic cancer cells were evaluated via cell viability and colony formation assays.

miR‑381 and miR‑489 suppress cell proliferation and invasion by targeting CUL4B via the Wnt/β‑catenin pathway in gastric cancer.

Accumulating evidence has highlighted the critical role of cullin 4B (CUL4B) in driving tumourigenesis in several malignancies, including gastric cancer (GC); however, the mechanisms underlying CUL4B upregulation remain unclear. The dysregulation of microRNAs (miRNAs or miRs) is known to be involved in tumourigenesis. In this study, we report that the expression of miR‑381 and miR‑489 is downregulated and is negatively correlated with that of CUL4B in GC tissues and cell lines.

, a crucial target of miR-410, functions as a potential oncogene in osteosarcoma.

Purpose: Mounting evidence highlights the essential role of in tumor initiation and malignant progression in several cancers; however, the function of in osteosarcoma (OS) remains unknown. In this study, we aim to investigate the role of and reveal its regulation by deregulated miRNAs in OS.

Materials And Methods: The expression profiles of were examined by immunohistochemistry, Western blotting, and qRT-PCR.

SPIN1 promotes tumorigenesis by blocking the uL18 (universal large ribosomal subunit protein 18)-MDM2-p53 pathway in human cancer.

Ribosomal proteins (RPs) play important roles in modulating the MDM2-p53 pathway. However, less is known about the upstream regulators of the RPs. Here, we identify SPIN1 (Spindlin 1) as a novel binding partner of human RPL5/uL18 that is important for this pathway.

Cancer-mutated ribosome protein L22 (RPL22/eL22) suppresses cancer cell survival by blocking p53-MDM2 circuit.

Several ribosomal proteins (RPs) in response to various ribosomal stressors have been shown to play a critical role in p53-dependent regulation of cell cycle arrest, apoptosis and tumor suppression. Here, we report ribosomal protein L22 (RPL22/eL22) as a novel p53 activator highly mutated (mostly deletion mutation) in various types of human cancers, but not essential for ribosomal biogenesis in normal cells. Ectopic expression of RPL22/eL22 suppressed the colony formation of cancer cells in a p53-dependent manner, whereas knockdown of RPL22/eL22 significantly compromised p53 activation by Actinomycin D, rescuing p53-induced G1/G0 cell cycle arrest.

TRIM24 promotes the aggression of gastric cancer via the Wnt/β-catenin signaling pathway.

Tripartite motif-containing 24 (TRIM24) is important in tumor development and progression. However, the role of TRIM24 in gastric cancer (GC) and the mechanisms underlying the dysregulated expression of TRIM24 remain to be fully elucidated. In the present study, it was found that TRIM24 was frequently overexpressed in GC cell lines and tissues compared with normal controls, as determined by western blotting and immunohistochemical staining.

promotes cell invasion in gastric cancer by activating the NF-κB signaling pathway.

() overexpression has been reported to be involved in the carcinogenesis and progression of many malignant tumors. However, the role of in the progression of gastric cancer (GC) remains unclear. In this study, we explored whether and how regulates proinflammatory signaling to promote GC cell invasion.

Regulation of TRIM24 by miR-511 modulates cell proliferation in gastric cancer.

Background: Increasing evidence highlights the important roles of tripartite motif containing 24 (TRIM24) in tumor initiation and malignant progression in many tumors, including gastric cancer (GC). Although TRIM24 expression is remarkably upregulated during GC carcinogenesis, the molecular mechanisms underlying TRIM24 dysregulation remain unexplored.

Methods: In this study, miRNA target prediction tools were applied to explore miRNAs that potentially target TRIM24.

CUL4A functions as an oncogene in ovarian cancer and is directly regulated by miR-494.

Cullin 4A (CUL4A), as a well-defined oncogene, has been reported to be upregulated in ovarian cancer clinically. However, the biological functions of CUL4A and the molecular mechanism underlying its upregulation in ovarian cancer remains unknown throughly. Here, we show that expression of CUL4A is significantly higher in ovarian cancer tissues compared to corresponding non-cancerous tissues.