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1.
Medicine (Baltimore) ; 103(27): e38797, 2024 Jul 05.
Artigo em Inglês | MEDLINE | ID: mdl-38968487

RESUMO

RATIONALE: Pulmonary sarcomatoid carcinoma (PSC), a rare tumor, comprises 0.1% to 0.4% of all malignant lung tumors. Given the rarity of PSC, its clinical course, therapeutic guidelines, and patient outcomes remain largely unknown. Therefore, it is imperative to alert clinicians to this extremely rare and instructive early-onset cancer. PATIENT CONCERNS: This report describes a 28-year-old woman with PSC, who was initially misdiagnosed with Whipple's disease. A conclusive diagnosis of PSC was made following careful clinical examination, imaging, and histopathological evaluation of the patient's biopsy sample. Radiological imaging revealed multiple nodules and mass formations in the left upper lobe of the patient's lung, with the largest measuring of 5.4 × 3.2 cm. DIAGNOSIS: Histopathological examination indicated the presence of a malignant neoplasm associated with necrosis suggestive of sarcoma, which was pathologically staged as cT4N1M1. INTERVENTIONS AND OUTCOMES: A regimen of doxorubicin and ifosfamide was administered therapeutically, resulting in a stable disease state. LESSONS: The rarity and tumor origin challenge the diagnosis, which emphasizes the imperative role of histological examination, immunohistochemistry, and flow cytometry in achieving an accurate diagnosis. This report summarizes the existing publications to provide a comprehensive overview of PSC, including its clinical manifestations, radiographic imaging, pathologic features, diagnostic challenges, treatment strategies, and prognosis, and aims to improve the understanding of PSC.


Assuntos
Neoplasias Pulmonares , Humanos , Feminino , Neoplasias Pulmonares/diagnóstico , Neoplasias Pulmonares/patologia , Adulto , Diagnóstico Diferencial , Sarcoma/diagnóstico , Sarcoma/patologia , Carcinossarcoma/diagnóstico , Carcinossarcoma/patologia
2.
Front Physiol ; 15: 1389113, 2024.
Artigo em Inglês | MEDLINE | ID: mdl-38803365

RESUMO

Gastrointestinal motility symptoms may be closely related to thyroid diseases. Sometimes, such symptoms are the only thyroid disease-related clue although the degree of the symptoms may vary. The exact mechanism of action of thyroid hormones on gastrointestinal motility is not completely understood, however, a clue lies in the fact that muscle cell receptors can be directly acted upon by thyroxines. Both hypo- and hyperthyroidism can cause impairment of gastrointestinal motility, modifying structure and function of pharynx and esophagus, and regulating esophageal peristalsis through neuro-humoral interaction. In hyperthyroid patients, alterations of postprandial and basic electric rhythms have been observed at gastro-duodenal level, often resulting in slower gastric emptying. Gastric emptying may also be delayed in hypothyroidism, but an unrelated gastric mucosa-affecting chronic modification may also cause such pattern. Hyperthyroidism commonly show malabsorption and diarrhoea, while hypothyroidism frequently show constipation. In summary, it can be stated that symptoms of gastrointestinal motility dysfunction can be related to thyroid diseases, affecting any of the gastrointestinal segment. Clinically, the typical thyroid disease manifestations may be missing, borderline, or concealed because of intercurrent sicknesses. Motility-linked gastrointestinal problems may easily conceal a misdetected, underlying dysthyroidism that should be carefully analyzed. Here, we aim to elaborate on the associations between thyroid disorders and GI dysmotility and the common clinical manifestations associated with GI dysmotility.

3.
Crit Rev Eukaryot Gene Expr ; 33(4): 53-61, 2023.
Artigo em Inglês | MEDLINE | ID: mdl-37183946

RESUMO

INTRODUCTION: The objective of this research is to explore whether LncRNA RP11 23J9.4 can be used as a targeted marker for the treatment of thyroid cancer (TC), downregulation of LncRNA RP11 23J9.4 and X-ray radiation have synergistic inhibitory effect on TC. METHODS: The expression of LncRNA RP11 23J9.4 in papillary thyroid carcinoma (PTC) cell was downregulated by cell transfection, and its inhibitory effect on PTC cells was proved through proliferation, invasion experiment, apoptosis, and cell cycle analysis. The transfected cells were irradiated with 2 Gy X-ray. The above methods were also used to detect whether they had synergistic inhibitory effect on TC. The expression of Axin2 gene and protein were detected by real-time PCR, Western blotting, and immunohistochemistry. RESULTS: On the one hand, it is proved that downregulating the expression of LncRNA RP11 23J9.4 can inhibit the development of TC through Axin2. On the other hand, it is clear that downregulation of LncRNA RP11 23J9.4 and X-ray radiation have synergistic inhibitory effect on TC. CONCLUSIONS: LncRNA RP11 23J9.4 and X-ray have significant synergistic effect on TC. LncRNA RP11 23J9.4 can be used as a marker for TC targeted therapy.


Assuntos
RNA Longo não Codificante , Neoplasias da Glândula Tireoide , Humanos , RNA Longo não Codificante/genética , RNA Longo não Codificante/metabolismo , Linhagem Celular Tumoral , Proliferação de Células/genética , Regulação Neoplásica da Expressão Gênica , Neoplasias da Glândula Tireoide/genética , Neoplasias da Glândula Tireoide/metabolismo , Câncer Papilífero da Tireoide/genética , Movimento Celular/genética
4.
Front Biosci (Landmark Ed) ; 28(4): 71, 2023 04 06.
Artigo em Inglês | MEDLINE | ID: mdl-37114538

RESUMO

Long noncoding RNAs (lncRNAs) are RNA molecules with a length of more than 200 nt that have been discovered in recent years. LncRNAs can participate in regulating gene expression and various biological activities through multiple pathways, such as at the epigenetic level, transcriptional level, and posttranscriptional level. In recent years, with the increasing understanding of lncRNAs, a large number of studies have shown that lncRNAs are closely related to ovarian cancer and participate in its occurrence and development, providing a new method to investigate ovarian cancer. In this review, we analyzed and summarized the relationship between various lncRNAs and ovarian cancer in terms of occurrence, development, and clinical significance, in order to provide a theoretical basis for basic research and clinical application of ovarian cancer.


Assuntos
Neoplasias Ovarianas , RNA Longo não Codificante , Humanos , Feminino , RNA Longo não Codificante/genética , RNA Longo não Codificante/metabolismo , Regulação Neoplásica da Expressão Gênica , Neoplasias Ovarianas/genética , Neoplasias Ovarianas/metabolismo , Relevância Clínica , Epigenômica
5.
Am J Cancer Res ; 8(3): 435-449, 2018.
Artigo em Inglês | MEDLINE | ID: mdl-29636999

RESUMO

Substantial evidence has shown that numerous microRNAs (miRNAs) are deregulated in colorectal cancer (CRC) and that their dysregulation is involved in CRC formation and progression. miRNA-based targeted therapy that inhibits or restores expression may be a promising therapeutic approach for anti-cancer therapy. Therefore, a comprehensive investigation of the mechanisms underlying CRC occurrence and development may help identify effective therapeutic targets for the therapy of CRC, thus improving the prognosis of patients with this disease. This study showed that miRNA-532 (miR-532) was significantly down-regulated in CRC tissues and cell lines. Low miR-532 expression strongly correlated with aggressive clinicopathological characteristics, including tumor size, lymphatic metastasis and TNM stage. Exogenous expression of miR-532 restricted cell proliferation, colony formation, migration and invasion; promoted cell apoptosis in vitro; and reduced tumor growth in vivo. Mechanistically, insulin-like growth factor 1 receptor (IGF-1R) was determined to be a novel direct target gene of miR-532 in CRC. In clinical CRC tissues, the expression of miR-532 was inversely correlated with that of IGF-1R, which was clearly overexpressed in CRC tissues. Furthermore, IGF-1R silencing simulated the tumor-suppressing roles of miR-532 in CRC. Moreover, recovered IGF-1R expression antagonized the inhibitory effects of miR-532 overexpression on CRC cells. Notably, miR-532 overexpression inhibited activation of the PI3K/Akt signaling pathway in CRC, both in vitro and in vivo. These results indicate that miR-532 plays an important role in CRC development, partly by directly targeting IGF-1R and regulating the PI3K/Akt signaling pathway. Thus, the miR-532/IGF-1R axis has clinical significance in the therapy of patients with CRC.

6.
Cancer Med ; 6(6): 1301-1310, 2017 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-28440026

RESUMO

Although the molecular biology of GC has been well characterized, early diagnostic biomarkers and effective therapeutic options in gastric cancer are still under investigation. Here, we found that miR-148b expression decreased in human gastric cancer tissues compared with matched adjacent nontumor tissues by q-PCR analysis and in situ hybridization. Further investigation revealed that overexpression of miR-148b limited glycolysis including glucose consumption, lactate production in gastric cancer cell lines BGC-823 and MKN45. Bioinformatics prediction uncovered that a dedicated transporters solute carrier family 2 member 1 (SLC2A1), also called GLUT1, was the direct target of miR-148b. The target effects were further confirmed by luciferase assay and western blot analysis. Besides, a reverse correlation was observed between relative SLC2A1 and miR-148b expression in human GC tissues compared with matched adjacent nontumor tissues. Subsequently, SLC2A1 suppression by SLC2A1 siRNA or specific inhibitor restricted the reduced effects of glycolysis mediated by miR-148b while SLC2A1 overexpression abrogated the effect of miR-148b on glycolysis. Our findings provided new evidence of miR-148b in GC development through restraining glycolysis, highlighting the role of miR-148b as a new target for GC treatment.


Assuntos
Transportador de Glucose Tipo 1/metabolismo , Glicólise , MicroRNAs/metabolismo , Neoplasias Gástricas/metabolismo , Trifosfato de Adenosina/metabolismo , Linhagem Celular , Proliferação de Células , Regulação para Baixo , Glucose/metabolismo , Transportador de Glucose Tipo 1/genética , Humanos , Ácido Láctico/metabolismo , MicroRNAs/genética , RNA Interferente Pequeno/genética , Neoplasias Gástricas/genética
7.
Gene ; 504(2): 262-7, 2012 Aug 10.
Artigo em Inglês | MEDLINE | ID: mdl-22565189

RESUMO

Med19 was a member of the Mediator complex which forms the bridge between transcriptional activators and RNA polymerase II. We aim to investigate the functional role of Med19 in the progression of human gastric carcinoma. The correlation between Med19 expression and clinicopathologic features in 60 gastric carcinoma specimens was analyzed by using immunohistochemistry. Recombinant lentivirus expressing Med19 short hairpin RNA (shRNA) was constructed and infected into human gastric carcinoma SGC7901 and MGC803 cells. MTT, colony formation and cell cycle analysis were used to study the effect of Med19 shRNA on gastric cancer cell proliferation. Expression of Med19 was associated with tumor size, cancer cell differentiation, and TNM stages (P<0.05). Downregulation of Med19 significantly inhibited cell proliferation and colony-formation capacity, and induced G1 phase cell-cycle arrest. Collectively, Med19 functions in promoting cellular growth and may be a useful therapeutic target in malignant gastric carcinoma.


Assuntos
Complexo Mediador/fisiologia , Neoplasias Gástricas/patologia , Linhagem Celular Tumoral , Progressão da Doença , Técnicas de Silenciamento de Genes , Humanos , Imuno-Histoquímica , Complexo Mediador/genética
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