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The emergence of spatial multi-omics has helped address the limitations of single-cell sequencing, which often leads to the loss of spatial context among cell populations. Integrated analysis of the genome, transcriptome, proteome, metabolome, and epigenome has enhanced our understanding of cell biology and the molecular basis of human diseases. Moreover, this approach offers profound insights into the interactions between intracellular and intercellular molecular mechanisms involved in the development, physiology, and pathogenesis of human diseases. In this comprehensive review, we examine current advancements in multi-omics technologies, focusing on their evolution and refinement over the past decade, including improvements in throughput and resolution, modality integration, and accuracy. We also discuss the pivotal contributions of spatial multi-omics in revealing spatial heterogeneity, constructing detailed spatial atlases, deciphering spatial crosstalk in tumor immunology, and advancing translational research and cancer therapy through precise spatial mapping. [ABSTRACT FROM AUTHOR]

Docosahexaenoic acid (DHA) supplementation is recommended for women during pregnancy because of its neurological, visual, and cognitive effects. Previous studies have suggested that DHA supplementation during pregnancy may prevent and treat certain pregnancy complications. However, there are contradictions in the current related studies, and the specific mechanism by which DHA acts remains unclear. This review summarizes the research on the relationship between DHA intake during pregnancy and preeclampsia, gestational diabetes mellitus, preterm birth, intrauterine growth restriction, and postpartum depression. Furthermore, we explore the impact of DHA intake during pregnancy on the prediction, prevention, and treatment of pregnancy complications as well as its impact on offspring neurodevelopment. Our results suggest that there is limited and controversial evidence for the protective effect of DHA intake on pregnancy complications, with the exception of preterm birth and gestational diabetes mellitus. However, additional DHA supplementation may improve long-term neurodevelopmental outcomes in the offspring of women with pregnancy complications. [ABSTRACT FROM AUTHOR]

Integration of human papilloma virus (HPV) DNA into the human genome may progressively contribute to cervical carcinogenesis. To explore how HPV integration affects gene expression by altering DNA methylation during carcinogenesis, we analyzed a multiomics dataset for cervical cancer. We obtained multiomics data by HPV‐capture sequencing, RNA sequencing, and Whole Genome Bisulfite Sequencing from 50 patients with cervical cancer. We detected 985 and 485 HPV‐integration sites in matched tumor and adjacent paratumor tissues. Of these, LINC00486 (n = 19), LINC02425 (n = 11), LLPH (n = 11), PROS1 (n = 5), KLF5 (n = 4), LINC00392 (n = 3), MIR205HG (n = 3) and NRG1 (n = 3) were identified as high‐frequency HPV‐integrated genes, including five novel recurrent genes. Patients at clinical stage II had the highest number of HPV integrations. E6 and E7 genes of HPV16 but not HPV18 showed significantly fewer breakpoints than random distribution. HPV integrations occurring in exons were associated with altered gene expression in tumor tissues but not in paratumor tissues. A list of HPV‐integrated genes regulated at transcriptomic or epigenetic level was reported. We also carefully checked the candidate genes with regulation pattern correlated in both levels. HPV fragments integrated at MIR205HG mainly came from the L1 gene of HPV16. RNA expression of PROS1 was downregulated when HPV integrated in its upstream region. RNA expression of MIR205HG was elevated when HPV integrated into its enhancer. The promoter methylation levels of PROS1 and MIR205HG were all negatively correlated with their gene expressions. Further experimental validations proved that upregulation of MIR205HG could promote the proliferative and migrative abilities of cervical cancer cells. Our data provides a new atlas for epigenetic and transcriptomic regulations regarding HPV integrations in cervical cancer genome. We demonstrate that HPV integration may affect gene expression by altering methylation levels of MIR205HG and PROS1. Our study provides novel biological and clinical insights into HPV‐induced cervical cancer. [ABSTRACT FROM AUTHOR]

Persistent HPV infection is recognized as the main etiologic factor for cervical cancer. HPV expresses the oncoproteins E6 and E7, both of which play key roles in maintaining viral infection and promoting carcinogenesis. While siRNA- mediated targeting of E6 and E7 transcripts temporarily induces apoptosis in HPV-positive cells, it does not eliminate viral DNA within the host genome, which can harbor escape mutants. Here, we demonstrated that specifically targeting E6 and E7 within host DNA with transcription activator-like effector nucleases (TALENs) induces apoptosis, inhibits growth, and reduces tumorigenicity in HPV-positive cell lines. TALEN treatment efficiently disrupted E6 and E7 oncogenes, leading to the restoration of host tumor suppressors p53 and retinoblastoma 1 (RB1), which are targeted by E6 and E7, respectively. In the K14-HPV16 transgenic mouse model of HPV-driven neoplasms, direct cervical application of HPV16-E7-targeted TALENs effectively mutated the E7 oncogene, reduced viral DNA load, and restored RB1 function and downstream targets transcription factor E2F1 and cycling-dependent kinase 2 (CDK2), thereby reversing the malignant phenotype. Together, the results from our study suggest that TALENs have potential as a therapeutic strategy for HPV infection and related cervical malignancy., Introduction Cervical cancer remains the third most common cancer in women worldwide, with approximately 529,800 new cases and 275,100 deaths annually (1, 2). HPVs, especially HPV16 and HPV18, are the [...]

Cervical carcinoma is a serious type of gynecological cancer that can affect women of all ages. Cervical carcinoma presents challenges for precision medicine, as not all tumors have specific gene mutations or alterations that can be targeted with existing drugs. Nonetheless, there are some promising targets in cervical carcinoma. Herein, genomic mutation data from The Cancer Genome Atlas and Catalogue of Somatic Mutations in Cancer were used to identify genomic targets for cervical carcinoma. PIK3CA was the most mutant gene among the promising targets, especially in cervical squamous cell carcinoma, and the mutated genes of cervical carcinoma were enriched in the RTK/PI3K/MAPK and Hippo pathways. In vitro, PIK3CA‐mutant cervical cancer cell lines showed higher sensitivity to Alpelisib than cancer cells without the PIK3CA mutation and the normal cells (HCerEpic). Protein–protein networks and co‐immunoprecipitation of PIK3CA revealed reduced interaction between p110α and ATR in PIK3CA‐mutant cervical cancer cells, which were sensitive to the combination of Alpelisib and cisplatin in vivo. Furthermore, Alpelisib significantly suppressed the proliferation and migration of PIK3CA‐mutant cervical cancer cells via inhibition of the AKT/mTOR pathway. Overall, Alpelisib showed antitumor effects and enhance cisplatin efficacy in PIK3CA‐mutant cervical cancer cells via PI3K/AKT pathways. Our study demonstrated the therapeutic potential of Alpelisib in PIK3CA‐mutant cervical carcinoma, which provides insights into precision medicine in cervical carcinoma. [ABSTRACT FROM AUTHOR]

Human papillomavirus (HPV) integration and high expression of HPV oncogenes (E6 and E7) are important mechanisms for HPV carcinogenesis in cervical cancer. However, the relationship between HPV integration and HPV E6 spliced transcripts, as well as the underlying mechanisms of HPV integration in carcinogenesis after HPV E6 splicing remains unclear. We analyzed HPV‐coiled‐coil domain containing 106 (CCDC106) integration samples to characterize the roles of HPV integration, E6 spliceosome I (E6*I), and high CCDC106 expression in cervical carcinogenesis. We found that E6 was alternatively spliced into the E6*I transcript in HPV‐CCDC016 integration samples with low p53 expression, in contrast to the role of E6*I in preventing p53 degradation in cervical cancer cells. In addition, CCDC106 was highly expressed after HPV‐CCDC106 integration, and interacted with p53, resulting in p53 degradation and cervical cancer cell progression in vitro and in vivo. Importantly, when E6*I was highly expressed in cervical cancer cells, overexpression of CCDC106 independently degraded p53 and promoted cervical cancer cell progression. In this study, we explored the underlying mechanisms of HPV‐CCDC106 integration in HPV carcinogenesis after HPV E6 splicing, which should provide insight into host genome dysregulation in cervical carcinogenesis. [ABSTRACT FROM AUTHOR]

The effective treatment of advanced cervical cancer remains challenging. Herein, single‐nucleus RNA sequencing (snRNA‐seq) and SpaTial enhanced resolution omics‐sequencing (Stereo‐seq) are used to investigate the immunological microenvironment of cervical squamous cell carcinoma (CSCC). The expression levels of most immune suppressive genes in the tumor and inflammation areas of CSCC are not significantly higher than those in the non‐cancer samples, except for LGALS9 and IDO1. Stronger signals of CD56+ NK cells and immature dendritic cells are found in the hypermetabolic tumor areas, whereas more eosinophils, immature B cells, and Treg cells are found in the hypometabolic tumor areas. Moreover, a cluster of pro‐tumorigenic cancer‐associated myofibroblasts (myCAFs) are identified. The myCAFs may support the growth and metastasis of tumors by inhibiting lymphocyte infiltration and remodeling of the tumor extracellular matrix. Furthermore, these myCAFs are associated with poorer survival probability in patients with CSCC, predict resistance to immunotherapy, and might be present in a small fraction (< 30%) of patients with advanced cancer. Immunohistochemistry and multiplex immunofluorescence staining are conducted to validate the spatial distribution and potential function of myCAFs. Collectively, these findings enhance the understanding of the immunological microenvironment of CSCC and shed light on the treatment of advanced CSCC. [ABSTRACT FROM AUTHOR]

Lysyl oxidase-like 2 (LOXL2) is a member of the lysine oxidase (LOX) family. Although its overexpression is known to play pivotal roles in carcinogenesis, its involvement in cervical cancer remains undefined. Here, we comprehensively explored the expression level and functional mechanism of LOXL2 in cervical cancer using bioinformatics and experimental methods. Bioinformatics analysis revealed that LOXL2 was significantly upregulated in cervical cancer compared to normal tissues. Enrichment analysis showed that most positively or negatively correlated genes of LOXL2 were correlated with extracellular matrix (ECM) formation and epithelial-mesenchymal transition (EMT). Further experiments confirmed that overexpression of LOXL2 greatly enhanced the malignant transformation abilities (e.g. proliferation, invasion, and migration) of cervical cancer cells via mediation of EMT. Furthermore, the small molecule inhibitor of LOXL2 ((2-Chloropyridin-4-yl) methanamine hydrochloride) significantly decreased the invasive ability of cervical cancer by reversing the process of LOXL2-induced EMT. In summary, LOXL2 may be a promising diagnostic and therapeutic biomarker for cervical cancer, and its small molecule inhibitor may be an effective anti-tumor drug. Abbreviations: LOXL2 Lysyl oxidase-like 2; LOX lysine oxidase; CI confidence interval; HR hazard ratio; ECM extracellular matrix; EMT epithelial-mesenchymal transition; OS overall survival; IC50 median inhibitory concentration; PPI protein-protein interaction. [ABSTRACT FROM AUTHOR]

We explored the role of HPV in the development of CIN into cervical cancer from an individual evolution perspective to reveal the underlying molecular changes and mechanisms related to HPV-induced carcinogenesis. (A) Hotspot genes of HPV integration at normal (HPV+), CIN and tumour stages. [Extracted from the article]

Human papillomavirus (HPV) integration in the human genome is suggested to be an important cause of cervical cancer. With the development of sequencing technologies, an increasing number of integration "hotspots" have been identified. However, this HPV integration information was derived from analysis of whole cervical cancer tissue, and we know very little about the integration in different cancer cell subgroups or individual cancer cells. This study optimized the preparation of probes and provided a dual-color fluorescence in situ hybridization (FISH) method to detect HPV integration sites in paraffin-embedded cervical cancer samples. We used both HPV probes and site-specific probes: 3p14 (FHIT), 8q24 (MYC), 13q22 (KLF5 / KLF12), 3q28 (TP63), and 5p15 (TERT). We detected HPV signals in 75 of the 96 cases of cervical cancer; 62 cases showed punctate signals, and 13 cases showed diffuse punctate signals. We identified 3p14 as a high-frequency HPV integration site in 4 cervical cancer cases. HPV integration at 8p14 occurred in 2 cases of cervical cancer. In the same cervical cancer tissue of sample No.1321, two distinct subgroups of cells were observed based on the HPV probe but showed no difference in cell and nucleus morphology. Our study provides a new method to investigate the frequent HPV integration sites in cervical cancer and reports the heterogeneity within cervical cancer from the perspective of HPV integration. [ABSTRACT FROM AUTHOR]

Background: Mitochondrial calcium uniporter regulator 1 (MCUR1, also known as CCDC90A) is a protein-coding gene that plays a key role in mitochondrial calcium uptake. However, knowledge about its clinical significance in breast cancer is still limited. Methods: The expression profile of MCUR1 in various cancers was analyzed via the ONCOMINE and Tumor Immune Estimation Resource databases. The correlation between MCUR1 expression and the clinical features of breast cancer was investigated using UALCAN and MEXPRESS. Immunohistochemical analysis was applied to verify the expression of MCUR1 in breast cancer. The prognostic significance of MCUR1 in breast cancer was evaluated using Kaplan–Meier plotter and the PrognoScan database. Gene Set Enrichment Analysis (GSEA) was performed to explore the possible biological functions of MCUR1. In addition, the function of MCUR1 was examined by gene silencing in vitro. Western blotting was applied to detect the expression of proteins. Results: MCUR1 was overexpressed in breast cancer and significantly related to the clinical characteristics of breast cancer. Results from the public databases and IHC analysis indicated that MCUR1 expression was the highest in triple-negative breast cancer (TNBC). The high expression of MCUR1 was associated with poor overall survival, distant metastasis-free survival, and recurrence-free survival. GSEA showed that the hypoxia pathway, cellular reactive oxygen species (ROS) pathway, epithelial–mesenchymal transition pathway, and notch signaling pathway were differentially enriched in the high MCUR1 expression phenotype. In vitro experiments showed that MCUR1 knockdown in TNBC cell lines led to a decrease in cellular ROS and weakened cell migration and invasion abilities. Moreover, Western blotting showed that MCUR1 knockdown inhibited the epithelial–mesenchymal transition of TNBC cells via the ROS/Nrf2/Notch pathways. Conclusion: Our study suggests that MCUR1 plays a pivotal role in the malignant progression of breast cancer. [ABSTRACT FROM AUTHOR]

Objectives: This study aimed to assess the effect of neoadjuvant chemotherapy (NACT) on the rate of lymph node metastasis (LNM) in FIGO stage IB1-IIB cervical cancer patients and compare the LNM between NACT plus surgery and surgery only. Methods: We identified 34 eligible studies in PubMed, Web of Science, Cochrane Library, and EMBASE from inception to July 27, 2019. Data analyses were performed by Stata (version 13) and Revman (version 5.3). Results: In these 34 included studies, the pooled incidence of LNM was estimated as 23% (95% CI, 0.20-0.26; I2 = 79.6%, P <0.001). In the subgroup analysis, we identified five factors, including study type, year of publication, continents from which patients came, histological type and the FIGO stage. When taking FIGO stage into consideration, the LNM rate was 13% in stage IB (95% CI: 0.10-0.15; I2 = 5.5%, P =0.385), 23% in stage IIA (95% CI: 0.18-0.28; I2 = 0%, P =0.622), and 27% in stage IIB (95% CI: 0.20-0.33; I2 = 0%, P =0.898), respectively. Through the comparison between NACT plus surgery and surgery only based on the six randomized controlled trials, the incidence of positive lymph nodes was lower in patients receiving NACT plus surgery than surgery only (RR=0.57, 95% CI: 0.39-0.83; I2 = 60.5%, P =0.027). The 5-year OS was higher in the NACT + surgery group than surgery-only group (RR=1.13, 95% CI: 1.03-1.23; I2 = 0.0%, P =0.842). Conclusions: Among cervical cancer in stage IB1-IIB, the preoperative NACT plus radical surgery resulted in a 23% probability of LNM, which was lower than those receiving radical surgery only. In stage IIA and IIB, the effect of NACT to reduce LNM was more obvious. [ABSTRACT FROM AUTHOR]

To confirm the relationship between sex and the progression of Coronavirus Disease-19 (COVID-19), and its potential mechanism, among severe patients. For this retrospective study, we included 168 consecutive severe patients with pathogen-confirmed COVID-19 who were hospitalized between January 16th and February 4th, 2020, at Tongji Hospital in Wuhan, China. Clinical characteristics, laboratory parameters, and outcomes were compared and analyzed between males and females. In the present study, we analyzed 168 severe patients with COVID-19, including 86 males and 82 females, and 48 patients (28.6%) were diagnosed as critically ill. Of 86 male patients, 12.8% (11/86) died and 75.6% (65/86) were discharged; of 82 female patients, 7.3% (6/82) died and 86.6% (71/82) were discharged. Eleven laboratory parameters showed significant differences between male and female patients, and six of them were higher during the whole clinical course in patients who died than in patients who were discharged. In adjusted logistic regression analysis, males with comorbidities presented a higher risk of being critically ill than males without comorbidities (OR = 3.824, 95% CI = 1.279–11.435). However, this association attenuated to null in female patients (OR = 2.992, 95% CI = 0.937–9.558). A similar sex-specific trend was observed in the relation between age and critically ill conditions. We highlighted sex-specific differences in clinical characteristics and prognosis. Male patients appeared to be more susceptible to age and comorbidities. Sex is an important biological variable that should be considered in the prevention and treatment of COVID-19. Author summary: Overall, our results highlight sex-specific differences in clinical characteristics and prognosis to COVID-19, which are consistent with the sex-bias observed in other COVID-19 related studies. We also provided more evidence and explored the underlying mechanism with epidemiological analysis. Six candidate laboratory indicators with significant sex differences were considered as potential mediators affecting the prognosis of COVID-19. The age-specific risk distributions of COVID-19 showed a positive correlation between the prognosis and age/ comorbidities, which was significantly affected by sex. We also emphasize that sex is a biological variable that should be considered in the prevention and therapy of COVID-19. It is our hope that these methods may serve as a guide to the clinician in providing timely and specific therapy. Obviously, future studies are warranted to elucidate the different pathways and cellular responses between women and men. The key challenge is how best to use this disparity for providing adequate protection in both males and females. [ABSTRACT FROM AUTHOR]

Histone deacetylases (HDACs) have been linked to a variety of cancers, and HDAC inhibitors (HDACi) are a promising class of drugs that have demonstrated anti-cancer effects. However, we have little knowledge regarding the selection and application of HDAC inhibitors to the personalized treatment of ovarian cancer (OC). Here, we report a correlation between the high expression of HDACs and poor outcomes in OC patients, which reveals that HDACi are a class of agents that show great promise for the treatment of OC. Furthermore, we found that HDACi increased both the mRNA and protein levels of DHRS2, which has been shown to be closely linked to HDACi sensitivity when it is highly expressed, especially in ovarian cancer cells. Consistently, we found that suppression of DHRS2 reduced the sensitivity of OC cells to HDAC inhibitors via attenuation of the inhibitory effects of HDAC inhibitors on Mcl-1 in vitro. Our study demonstrated that DHRS2 expression was decreased in OC tissues and that high expression of DHRS2 was correlated with better outcomes in OC patients. In addition, DHRS2 expression was closely related to the effects of chemotherapy. Our study reveals the role of DHRS2 in cell apoptosis induced by HDAC inhibitors and explores the clinical attributes of DHRS2 in OC from a new perspective, suggesting that OC patients with high DHRS2 expression may benefit from treatment with HDAC inhibitors. [ABSTRACT FROM AUTHOR]

Cervical cancer is a serious threat to women's health and is the third most common malignancy in women worldwide. Recent studies indicate that the long non-coding RNA CCAT1 plays a role in the malignant behavior of many tumors. However, the role of CCAT1 in cervical cancer is still unknown. Our aim is to evaluate the expression and investigate the regulatory role and potential mechanism of CCAT1 in cervical cancer. CCAT1 expression was measured by qRT-PCR. In addition, CCK-8 assays, colony formation assays, qRT-PCR assays, Transwell assays and xenograft experiments were performed to determine the role of CCAT1 in the proliferation and invasion in cervical cancer cells. The expression of CCAT1 in the cervical cancer tissues was higher than in the adjacent normal tissues. Overexpressing CCAT1 promoted cervical cancer cell proliferation, colony formation, and invasion in vitro. Elevated CCAT1 suppressed miR-181a expression, which was accompanied by an increased expression of MMP14 and HB-EGF. In contrast, knocking down CCAT1 resulted in increased expression of miR-181a, along with decreased expression of MMP14 and HB-EGF. Thus, CCAT1 is a key oncogenic lncRNA associated with cervical cancer and plays a role in promoting cervical cancer cell proliferation and invasion by regulating the miR-181a-5p/MMP14 axis. [ABSTRACT FROM AUTHOR]

Increasing amounts of crop residues are being returned to croplands. Understanding nitrogen (N) availability in crop residues under various N fertilization regimes is important in optimizing N management. Pot experiments were conducted to investigate the contribution, fate and residual effects of urea and maize residue-N using a 15N isotope technique. Four N regimes were tested: three basal–topdressing ratios of N applied as urea (100–0, 75–25, 50–50) and one basal application of 75% N as urea and 25% N as manure (75U+25M). An average of 31.4% wheat N uptake was derived from urea, 9.2% from maize residue, and 59.5% from the soil in the first season. During the growing stages of wheat, maize residue contributed 0.3–4.8% and 3.1–13.2% to soil mineral and microbial biomass N, respectively, and those originated from urea was 1.0–4.2% and 4.6–16.8%, respectively. Regarding the fate of urea and residue-N after the first season, 35.9% and 16.9% of urea-15N and residue-15N were recovered by wheat, 28.1% and 46.9% remained in the soil, and 36.0% and 36.2% were lost. The contribution of urea to crop N uptake and N recovery efficiency increased, while that of residue-N decreased with increasing proportion of topdressing N. Substituting 25% mineral N with manure decreased the urea-15N loss without negative effects on crop dry matter and N uptake. Residual urea-15N and maize residue-15N from the previous season contributed 3.9% and 3.0% to summer maize N uptake. Additionally, 29.3% of residue-15N remained in the soil after the second season, while only 18.6% of urea-15N remained. Our study suggests that fertilizer and crop residue are actively involved in soil N transformation and plant N nutrition, emphasizing the capacities of organic residues to sustainably supply nutrients. Considering the utilization of both N fertilizer and maize residue, we may suggest a 75–25 split in N fertilizer application, but more appropriate options need to be further assessed under different cropping systems. [ABSTRACT FROM AUTHOR]

Highlights • A meta-analysis was used to integrate yield and NUE from alternative fertilization practices under four rice types in China. • The eff ;ectiveness of organic fertilizer, straw return and secondary/micronutrient on rice yield was affected by rice type. • The highest nitrogen use efficiency among the alternative fertilization options was achieved by slow-release N fertilizer. • Decreases in chemical fertilizer input can be realized by applying slow-release fertilizer and organic substitution. Abstract Applying alternative fertilization practices instead of conventional fertilizers might improve rice yield and nutrient use efficiency in rice cropping systems. However, the results range widely among individual studies, making generalizations difficult. Here, we investigated five alternative fertilization options (slow-release nitrogen fertilizer, SRF; organic fertilizer, OF; straw return, SR; green manure, GM; secondary/micronutrient fertilizer, SMF) and performed a meta-analysis to quantify their effects on rice yield and nitrogen (N) use efficiency across different rice types in China. Yield responses were significantly positive under all alternative fertilization options relative to those obtained with conventional fertilization, and the magnitude of yield increase exhibited the following the order: OF (7.8%) > SRF (7.4%) > GM (6.7%) > SR (5.4%) > SMF (4.6%). Furthermore, the recovery efficiency (REN), agronomic efficiency (AEN), and the partial factor productivity of nitrogen (PFPN) were increased by 6.0–34.8%, 10.2–29.5%, and 4.7–6.9%, respectively under the alternative fertilization options relative to conventional fertilization. The application of SRF and SMF generated higher yield responses in single rice than in other rice types, whereas OF and SR application resulted in better performance in early and middle rice. The rice yield response was maximized when approximately 70% slow-release N was combined with approximately 30% conventional N according to the quadratic relationship between the percentage of slow-release N substituting conventional N and the yield response. It was estimated that the total N rate could be reduced by up to 32% without yield loss with the application of slow-release N fertilizer instead of conventional N fertilizer. When organic N fully or partially substituted inorganic N, yield response declined with increasing substitution level, and the substitution proportion needed to be controlled below 20% to maintain rice yield. The meta-analysis results clearly demonstrate that appropriate alternative fertilization options can increase both rice yield and nitrogen use efficiency, and that conventional chemical fertilizers can be partially replaced with alternative ones without negatively affecting rice productivity. [ABSTRACT FROM AUTHOR]

Linking potassium (K) balance to soil fertility creates a valuable indicator for sustainability assessment in agricultural land-use systems. It is crucial for the efficient use of K resources, food security and resource sustainability to realize soil K balance status in China. Therefore, temporal and spatial changes of K balance for farmland in China from 1980 to 2015 were analyzed at national and regional levels using statistical data and related parameters. At the national scale, K input increased from 6.78 Mt K2O in 1980 to 23.44 Mt K2O in 2015 with an average annual increment of 0.48 Mt K2O, and output changed from 8.10 Mt in 1980 to 21.31 Mt in 2015 with an average annual increment of 0.38 Mt K2O as well. On average, K balance was -24.17, -5.92, 21.31 and 19.50 kg K2O ha-1 in 1980s, 1990s, 2000s and 2010s, respectively. Moreover, the average balance of six regions was considerably different which were -21.37, 1.25, 13.70, -22.79, 99.22 and 7.18 kg K2O ha-1 from 1980 to 2015. The potassium use efficiency (KUE) decreased with time which were 127.09, 104.35, 87.69 and 89.69% in 1980s, 1990s, 2000s and 2010s, respectively, and the decline of slope could also reflect the variation tendency of KUE. Great variation of K balance across different regions demonstrated that fertilizer application and management practices need to be adjusted to local conditions. [ABSTRACT FROM AUTHOR]