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Spectroscopic evaluation of carcinogenesis in endometrial cancer.

ABSTRACT: Carcinogenesis is a multifaceted process of cancer formation. The transformation of normal cells into cancerous ones may be difficult to determine at a very early stage. Therefore, methods enabling identification of initial changes caused by cancer require novel approaches. Although physical spectroscopic methods such as FT-Raman and Fourier Transform InfraRed (FTIR) are used to detect chemical changes in cancer tissues, their potential has not been investigated with respect to carcinogenesis. The study aimed to evaluate the usefulness of FT-Raman and FTIR spectroscopy as diagnostic methods of endometrial cancer carcinogenesis. The results indicated development of endometrial cancer was accompanied with chemical changes in nucleic acid, amide I and lipids in Raman spectra. FTIR spectra showed that tissues with development of carcinogenesis were characterized by changes in carbohydrates and amides vibrations. Principal component analysis and hierarchical cluster analysis of Raman spectra demonstrated similarity of tissues with cancer cells and lesions considered precursor of cancer (complex atypical hyperplasia), however they differed from the control samples. Pearson correlation test showed correlation between cancer and complex atypical hyperplasia tissues and between non-cancerous tissue samples. The results of the study indicate that Raman spectroscopy is more effective in assessing the development of carcinogenesis in endometrial cancer than FTIR.

SUBMITTER: Depciuch J

PROVIDER: S-EPMC8079695 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Background: Our previous work determined the correlation between high nuclear expression of hepatoma-derived growth factor (HDGF) and clinicopathological data of endometrial cancer (EC); however, the modulatory mechanisms and biological role of HDGF in EC have not been reported. Methods: Lentiviral particles carrying human HDGF short hairpin RNA (shHDGF-1, -2, and -3) vector and plasmids for HDGF, DDX5, and β-catenin expression were, respectively introduced into EC cells to evaluate the effects and molecular mechanisms underlying EC cell proliferation, migration, invasion, and metastasis. Quantitative real time reverse transcription polymerase chain reaction (qRT-PCR) and western blotting were used to determine HDGF and DDX5 expression. Co-immunoprecipitation (co-IP), mass spectrometry, and an immunofluorescence co-localization study were conducted to explore the relationship between HDGF, DDX5, and β-catenin. Immunohistochemistry was used to analyze the clinical associations between HDGF and DDX5 in EC. Results: Knocking down HDGF expression significantly decreased EC cellular proliferation, migration, invasion in vitro, as well as tumorigenesis and metastasis in vivo. Conversely, HDGF overexpression reversed these effects. Stable knockdown-based HDGF suppression activated the PI3K/AKT signaling pathway, along with downstream β-catenin-mediated cell cycle and epithelial-mesenchymal transition signaling. Furthermore, co-IP combined with mass spectrometry and an immunofluorescence co-localization study indicated that HDGF interacts with DDX5, whereas β-catenin was associated with DDX5 but not HDGF. Overexpression of DDX5 reversed the suppression of shHDGF. Immunohistochemistry analysis showed that high expression of DDX5 constituted an unfavorable factor with respect to the clinicopathological characteristics of EC tissues and that HDGF and DDX5 high expression (HDGF+/DDX5+) led to a worse prognosis for patients with EC (P < 0.001). In addition, we found that the expression of HDGF and DDX5 was positively correlated in EC tissues (r = 0.475, P < 0.001). Conclusion: Our results provide novel evidence that HDGF interacts with DDX5 and promotes the progression of EC through the induction of β-catenin.

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Spectroscopic evaluation of carcinogenesis in endometrial cancer.

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