Honghong Dong’s research while affiliated with Air Force Engineering University and other places

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Publications (2)


Diagnosis and management of multiple primary lung cancer
  • Literature Review
  • Full-text available

October 2024

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7 Reads

Honghong Dong

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Yahui Tian

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Shaowei Xin

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[...]

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Multiple primary lung cancer (MPLC), can be categorized as synchronous multiple primary lung cancer (sMPLC) and metachronous multiple primary lung cancer (mMPLC), which are becoming increasingly common in clinical practice. A precise differential diagnosis between MPLC and intrapulmonary metastases (IPM) is essential for determining the appropriate management strategy. MPLC is primarily diagnosed through histology, imaging, and molecular methods. Imaging serves as an essential foundation for preoperative diagnosis, while histology is a critical tool for establishing a definitive diagnosis. As molecular biology advances, the diagnosis of MPLC has stepped into the era of molecular precision. Surgery is the preferred treatment approach, with stereotactic radiotherapy and ablation being viable options for unresectable lesions. Targeted therapy and immunotherapy can be considered for specific patients. A multidisciplinary team approach to evaluation and the application of combination therapy can benefit more patients. Looking ahead, the development of more authoritative guidelines will be instrumental in streamlining the diagnosis and management of MPLC.

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Fig. 1. TCF19 is an important tumor gene in lung cancer. A. Kaplan-Meier survival analysis of TCF19-overexpression and TCF19-underexpression lung cancer patients. B. Expression level of TCF19 in lung tumor tissues and Para-tumor tissues (TCGA database). C, D. TCF19 mRNA and protein levels in lung cancer patient tissue samples (P: Para-tumor tissues, T: Tumor tissues). Data are means ± SEM of three independent experiments. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 (Student's t-test).
Fig. 2. TCF19 overexpression promotes lung cancer cell growth and tumorigenicity in vitro. A. Colony-forming evaluated the effects of TCF19 overexpression on the growth and proliferation of H460. B. CCK8 evaluated the effects of TCF19 overexpression on the growth and proliferation of H460. C. Colony-forming evaluated the effects of TCF19 overexpression on the growth and proliferation of Hop62 cells. D. CCK8 evaluated the effects of TCF19 overexpression on the growth and proliferation of Hop62 cells. E. Colony-forming evaluated the effects of TCF19 knock-down on the growth and proliferation of PC-9 cells. F. CCK8 evaluated the effects of TCF19 knock-down on the growth and proliferation of PC-9 cells. G. Colony-forming evaluated the effects of TCF19 knock-down on the growth and proliferation of H446 cells. H. CCK8 evaluated the effects of TCF19 knock-down on the growth and proliferation of H446 cells. I. Soft-agar assay of H460 and Hop62 cells in the presence of TCF19. J. Soft-agar assay of PC-9 and H446 cells in the absence of TCF19. Data are means ± SEM of three independent experiments. * p < 0.05, **p < 0.01, *** p < 0.001, **** p < 0.0001 (Student's t-test).
Fig. 3. TCF19 promoted tumorigenesis in vivo. A. Schematics for the xenograft treatments of nude mice. 2 × 10 6 cells were subcutaneously inoculated into the right flank of 8-wk-old female nude mice fed with normal food or DOX food. B-D. Tumor growth curves (B) were calculated based on the monitoring data every other day after subcutaneously injecting Hop62-TCF19 cells into female nude mice. The xenograft tumors were dissociated, photographed (C), and weighed (D) at the end of the experiments. (n = 6). E-G. Tumor growth curves (E) were calculated based on the monitoring data every other day after subcutaneously injecting H446-shTCF19 cells into female nude mice. The xenograft tumors were dissociated, photographed (F), and weighed (G) at the end of the experiments. (n = 6, shGFP as control group and shTCF19 as TCF19 knock-down group). H. Schematics of intranasal instillation of retrovirus for forced expressing TCF19 in Dox inducible Tet-KRAS G12D / CC10rtTA lung cancer mouse model. (n = 6; mice fed with normal food as the control group, mice fed with DOX to induce TCF19 overexpression as TCF19 overexpression group). I. Ectopic expression of TCF19 promotes lung cancer formation in TetO-Kras G12D /CC10rtTA mouse model. J. Representative images of Hematoxylin and eosin (H&E) staining of the lung tissues obtained from lenti-control and lenti-TCF19 treated Kras G12D /CC10rtTA mice. Data are means ± SEM of three independent experiments. * p < 0.05, **p < 0.01, *** p < 0.001, **** p < 0.0001 (Student's t-test).
Fig. 4. TCF19 promoted lung cancer cell cycle progression. A. The cell cycle of H460-TCF19 cells was analyzed by flow cytometry. B. The cell cycle of Hop62-TCF19 cells was analyzed by flow cytometry. C, D. The expression of cyclin A1, cyclin E1, cyclin D1, CDK2, and TCF19 in H460-TCF19 and Hop62-TCF19 cells was detected by western blotting. Data are means ± SEM of three independent experiments. * p < 0.05, **p < 0.01, *** p < 0.001, **** p < 0.0001 (Student's t-test).
Fig. 5. TCF19 activated Raf/MEK/ERK pathway. A. Heatmap of mRNA expression of Hop62-TCF19 cells. Cells were extracted for RNA-sequencing analysis. B. KEGG enrichment analysis of signal pathways affected by TCF19. C. The effect of TCF19 on the key proteins of Raf/MEK/ERK signaling pathway in H460 and Hop62 cells by western blotting. D. The relationship between TCF19 and proteins related to Raf/MEK/ERK signaling pathway or cell cycle in clinical lung cancer tissue samples. Data are means ± SEM of three independent experiments. * p < 0.05, **p < 0.01, *** p < 0.001, **** p < 0.0001 (Student's t-test).

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TCF19 promotes cell proliferation and tumor formation in lung cancer by activating the Raf/MEK/ERK signaling pathway

May 2024

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34 Reads

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3 Citations

Translational Oncology

Objective This study aimed to investigate TCF19′s role in lung cancer development, specifically its involvement in the RAF/MEK/ERK signaling pathway. Methods Lung cancer tissue analysis revealed significant TCF19 overexpression. In vitro experiments using A549 and Hop62 cells with TCF19 overexpression demonstrated enhanced cell growth. Transgenic mouse models confirmed TCF19′s role in primary tumor development. Transcriptome sequencing identified altered gene expression profiles, linking TCF19 to RAF/MEK/ERK pathway activation. Functional assays elucidated underlying mechanisms, revealing increased phosphorylation of Raf1, MEK1/2, and ERK1/2. Inhibiting RAF1 or ERK through shRaf1 or ERK inhibitor reduced cell cycle-related proteins and inhibited TCF19-overexpressing cell growth. Results TCF19 was identified as an oncogene in lung carcinoma, specifically impacting the RAF/MEK/ERK pathway. Elevated TCF19 levels in lung cancer suggest targeting TCF19 or its associated pathways as a promising strategy for disease management. Conclusion This study unveils TCF19′s oncogenic role in lung cancer, emphasizing its modulation of the RAF/MEK/ERK pathway and presenting a potential therapeutic target for TCF19-overexpressing lung cancers.

Citations (1)


... Lung cancer remains a major killer worldwide [1][2][3][4][5] . Small cell lung cancer (SCLC) represents a highly aggressive and treatment-resistant form of lung cancer that occurs in roughly 15% of all cases [6,7] . ...

Reference:

Advancement Opportunities and Endeavor of Innovative Targeted Therapies for Small Cell Lung Cancer
TCF19 promotes cell proliferation and tumor formation in lung cancer by activating the Raf/MEK/ERK signaling pathway

Translational Oncology