IntroductionPsychological injuries in social work are on the rise in complex modern society. Some individuals are incurring both physical and psychological injuries. Often, psychological injuries are more miserable than physical injuries. To combat the psychological injury suffered by individuals involved in social work, authorities should mobilize support via social media and raise funds by this and other feasible means to cover the cost of care for these individuals. This study focuses on social media support and funding assistance that could play useful roles in helping to treat psychological injuries among social workers and their clients in China.MethodsA scoping review of academic and gray literature was undertaken to identify the different injuries involved in social work. Semi-structured interviews were carried out with 7 experts, including social workers, social media professionals, and social fund directors. Empirical studies on psychological injuries in social work provided examples in support of the policy advocacy reported in this paper.ResultsThe scoping review found diverse literature on the subject of psychological injury in social work over the past decade in China. Semi-structured interviews with experts indicate that social media support can alleviate psychological suffering and that funding assistance has a positive influence on assisting individuals coping with psychological injuries. The empirical cases support the plan to encourage more support from social media and funding sources.ConclusionPsychological injury is greatly influenced by social bias and discrimination. According to cases and actions are taken to mitigate the harm done, supportive social media strategies could greatly diminish the psychological injuries to social workers and their clients and help them avoid much suffering. This study finds that funding organizations could provide a new treatment mechanism—social media marketing strategies and functional activities—to help a large number of individuals with psychological injuries out of the disease trap in China.

Purpose: To determine the effect of Forkhead box P2 (FOXP2) on thyroid carcinoma cell growth and metastasis. Methods: Expression of FOXP2 in thyroid carcinoma cells was determined using quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and western blot. The 3-[4,5-dimethylthiazol-2-yl]- 2,5 diphenyl tetrazolium bromide (MTT) was applied to evaluate cell viability, while cell migration and invasion were assessed by wound healing and Transwell assays, respectively. Flow cytometry and western blot were conducted to investigate cell apoptosis. The underlying mechanisms were investigated using western blot assay. Results: Expression of FOXP2 was lower in primary thyroid carcinoma tissues than in normal tissues based on data from the TCGA database. Similarly, FOXP2 was lower in thyroid carcinoma cells at the mRNA and protein levels. Ectopic FOXP2 expression decreased cell viability, and retarded the migration and invasion of thyroid carcinoma cells. FOXP2 overexpression in thyroid carcinoma cells led to down-regulated expression of matrix metallopeptidase (MMP) 2, MMP 9, and proliferating cell nuclear antigen (PCNA), as well as induction of cell apoptosis. Moreover, FOXP2 overexpression resulted in enhanced Bax expression while Bcl-2 was reduced. Ectopic expression of FOXP2 decreased β-catenin, c-myc, and cyclin D1 in thyroid carcinoma cells. Conclusion: FOXP2 suppresses the proliferation and metastasis of thyroid carcinoma cells, but promotes apoptosis through suppression of the Wnt/β-catenin signaling pathway. These results provide an insight that may lead to the development of a novel potential therapeutic strategy for treating thyroid carcinoma.

Purpose: To investigate the role and mechanism of formin-like protein 1 (FMNL1) in breast cancer progression. Methods: Expression of FMNL1 in breast cancer cells was evaluated using quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and western blotting. Colony formation and CCK8 assays were performed to assess cell proliferation. Cell migration and invasion were determined using wound-healing and Transwell assays, respectively. Results: Data from UALCAN prediction (http://ualcan.path.uab.edu/analysis.html) showed that FMNL1 was significantly upregulated in primary breast cancer tissue compared to normal tissue (p < 0.01). Enhanced FMNL1 mRNA and protein expression was also identified in breast cancer cells. shRNA-mediated FMNL1 knockdown decreased viability of breast cancer cells and reduced cell proliferation, migration, and invasion. Expression of protein high mobility group AT-hook 1 (HMGA1) was reduced, whereas breast cancer gene 1 (BRCA1) expression was enhanced, in breast cancer cells transfected with shRNA-FMNL1. Overexpression of HMGA1 attenuated FMNL1-knockdown–induced decreased HMGA1 expression and increased BRCA1 expression in breast cancer cells. BRCA1 knockdown counteracted the suppressive effects of FMNL1 silencing on breast cancer cell proliferation, migration, and invasion. Conclusion: FMNL1 promotes breast cancer cell growth and metastasis by inhibiting BRCA1 via upregulation of HMGA1, providing a potential therapeutic target for breast cancer.

In the earlier published article, “Herbei Province” included in the affiliation of the second author is incorrect. “Chongqing” is a municipality directly under the Central Government and does not belong to "Hebei Province”. At the request of the author, the correct affiliation is provided above. New citation: Zhang Q, Yang H, Tang C, Wang Q, Ren L, Jia C, et al. FMNL1 promotes growth and metastasis of breast cancer by inhibiting BRCA1 via upregulation of HMGA1. Trop J Pharm Res 2021; 20(8):1559-1564 doi: 10.4314/tjpr.v20i8.2. Erratum: 2022; 21(8): 1807 doi: 10.4314/ tjpr.v 21i8.31 Earlier citation: Zhang Q, Yang H, Tang C, Wang Q, Ren L, Jia C, et al. FMNL1 promotes growth and metastasis of breast cancer by inhibiting BRCA1 via upregulation of HMGA1. Trop J Pharm Res 2021; 20(8):1559-1564 doi: 10.4314/tjpr.v20i8.2

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