MYCT1 inhibits hematopoiesis in diffuse large B-cell lymphoma by suppressing RUNX1 transcription.

BACKGROUND: The abnormality of chromosomal karyotype is one factor causing poor prognosis of lymphoma. In the analysis of abnormal karyotype of lymphoma patients, three smallest overlap regions were found, in which MYCT1 was located. MYCT1 is the first tumor suppressor gene cloned by our research team, but its studies relating to the occurrence and development of lymphoma have not been reported. METHODS: R banding analyses were employed to screen the abnormality of chromosomal karyotype in clinical specimen and MYCT1 over-expression cell lines. FISH was to monitor MYCT1 copy number aberration. RT-PCR and Western blot were to detect the mRNA and protein levels of the MYCT1 and RUNX1 genes, respectively. The MYCT1 and RUNX1 protein levels in clinical specimen were evaluated by immunohistochemical DAB staining. The interaction between MYCT1 and MAX proteins was identified via Co-IP and IF. The binding of MAX on the promoter of the RUNX1 gene was detected by ChIP and Dual-luciferase reporter assay, respectively. Flow cytometry and CCK-8 assay were to explore the effects of MYCT1 and RUNX1 on the cell cycle and proliferation, respectively. RESULTS: MYCT1 was located in one of three smallest overlap regions of diffuse large B-cell lymphoma, it altered chromosomal instability of diffuse large B-cell lymphoma cells. MYCT1 negatively correlated with RUNX1 in lymphoma tissues of the patients. MAX directly promoted the RUNX1 gene transcription by binding to its promoter region. MYCT1 may represses RUNX1 transcription by binding MAX in diffuse large B-cell lymphoma cells. MYCT1 binding to MAX probably suppressed RUNX1 transcription, leading to the inhibition of proliferation and cell cycle of the diffuse large B-cell lymphoma cells. CONCLUSION: This study finds that there is a MYCT1-MAX-RUNX1 signaling pathway in diffuse large B-cell lymphoma. And the study provides clues and basis for the in-depth studies of MYCT1 in the diagnosis, treatment and prognosis of lymphoma.

Chondrosarcoma of the toe: A case report and literature review.

BACKGROUND: Chondrosarcoma of the foot is a rare malignant bone tumour, and it is even rarer when it originates in a toe bone. Surgical excision is the only effective treatment. The osteolytic destruction of the tumour severely affects limb function and carries the risk of distant metastasis. Most such tumours are removed surgically to minimize local recurrence and distant metastases, maximize limb function, and prolong the patient's tumour-free survival time. The main objective of this article is to present the case of a chondrosarcoma that invaded the first phalanx of the left foot and formed a large phalangeal mass with osteolytic destruction of the distal bone. CASE SUMMARY: A 74-year-old man suffered from swelling of his left toe for six months, with pain and swelling for two months. Computed tomography and magnetic resonance imaging showed that the tumour on the first phalanx of the left foot was approximately 54.9 mm × 44.6 mm, surrounded by a significant soft tissue signal mass, with osteolytic destruction of the distal phalanx and a speckled bone-like high-density shadow within it. CONCLUSION: Chondrosarcoma occurring in a toe bone is extremely rare. In this case, extensive surgical resection of the large low-grade chondrosarcoma, which showed osteolytic destruction and invaded the distal metatarsal bone, was safe and effective.

miR-19a promotes cell growth and tumorigenesis through targeting SOCS1 in gastric cancer.

Accumulating evidence has shown that microRNAs are involved in cancer development and progression. However, it remains unknown about the potential role of miR-19a in the pathogenesis of gastric cancer. Here, we report that suppressor of cytokine signaling 1 (SOCS1) is a novel target of miR-19a in gastric cancer cells and that miR-19a expression is inversely correlated with SOCS1 expression in gastric cancer cells and a subset of gastric cancer tissues. Ectopic expression of miR-19a dramatically promoted proliferation and tumorigenicity of gastric cancer cells both in vitro and in vivo. Moreover, we showed that silencing of SOCS1 promoted cell growth and colony formation resembling that of miR-19a overexpression, whereas re-introduction of SOCS1 (without the 3'-UTR) attenuated the pro-tumorigenic functions. Taken together, our findings suggest that the SOCS1 gene is a direct target of miR-19a, which functions as an oncogenic miRNA in gastric cancer by repressing the expression of tumor suppressor SOCS1.